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For Biochemistry we had to write a 10-page paper on a disease associated with a metabolic pathway and list possible nutritional recommendations for that disease.  I chose Alzheimer’s Disease, and was astounded to read the latest research by Dr. Dale Bredesen documenting (with MRI brain scans, etc) how his protocol has reversed cognitive decline in hundreds of patients leading in many cases to complete regression and no signs of the disease.  Improvements in all cases have been maintained from the time of implementation of the protocol up until the present time, meaning around 5 years for a few patients.  This has gotten a tiny bit of media coverage in America, but I don’t know if it is being discussed in Germany: http://mariashriver.com/blog/2016/09/alzheimers-prevention-dale-bredesen-maria-shriver/ http://www.today.com/health/new-brain-program-may-fight-alzheimer-s-t104636  https://www.facebook.com/MariaShriver/videos/10156963263905455/  The subject is really complex, & this is really just an overview, but all the topics are cited in my reference section if you’d like to dive deeper.

If you’ve been confused about all the buzz over the future of Functional Medicine and its potential in combatting chronic disease, research into Dale Bredesen’s protocol will get you excited too.  So far 99% of his protocol involves no drugs – only lifestyle modifications and nutrition.

Maybe this information might encourage you to get your DNA genotyped from an organization like 23andme: https://www.23andme.com/  Certainly, knowing if you are ApoE4 homozygous or heterozygous is useful information in any prevention program.

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Part I. What the disease is:  symptoms, & in which type of population it’s most prevalent

Alzheimer’s Disease is still considered by most practitioners as a progressive neurodegenerative disease, where symptoms of dementia including memory and thinking skills worsen gradually and unstoppably over time5,12.  Survival after diagnosis averages 8 years, rendering patients by the end vacant-eyed and unable to respond to visitors or their environment12.  Alzheimer’s in 2016, was considered “the third leading cause of death in the United States, following only cardiovascular disease and cancer,” but another recent research review determined that many deaths from Alzheimer’s go unreported, meaning the total number of deaths significantly exceeds CDC’s estimations2,5.   Of the 318 million Americans living, it is estimated that 45 million (15% of the population) will get Alzheimers during their lifetime37.  But the incidence of Alzheimer’s has reached almost 50% in people over 85 years of age46.  Although it is the elderly population over 65 that generally gets a diagnosis of Alzheimer’s, clear symptoms of the disease’s predecessors including mild cognitive impairment (MCI) and subjective cognitive impairment (SCI) can be observed 20 years previously, and can be successfully addressed and often reversed at that time31

There is a very recent model of Alzheimer’s Disease promoted by Dale E. Bredesen, PhD who describes it not as “a progressive and…irreversible neurodegenerative disease” (like most research papers in the last decade describe it), but as “the body’s protective response to several metabolic and toxic insults”, which can mechanistically be reversed, especially when caught in its early stages1,7.  Due to the fact that Dr. Bredesen’s group is the only group showing documented, objective, and peer-reviewed success in treating Alzheimers, this report focuses on theories he supports from causal microbiome vulnerability to the molecular mechanism behind neurodegeneration, and multifaceted therapies for treatment.  The peer-reviewed research that backs up Dr. Bredesen’s theories that are cited following this report’s conclusion, represent only a small fraction of a massive volume performed on Alzheimer’s in the last two decades. 

Dr. Bredesen is currently the Director, Mary S. Easton Center for Alzheimer’s Research  and founder/CEO of the Buck Institute for Research on Aging, and champions the metabolic enhancement for neurodegeneration (MEND) therapeutic approach (allied with Functional Medicine ideals), which has achieved radical success in not only halting the progress of Alzheimer’s, but in reversing its destruction and bringing in many cases normal cognitive function back not only to individuals experiencing Mild Cognitive Impairment (MCI) and Subjective Cognitive Impairment (SCI) pre-Alzheimer’s conditions, but also to individuals in early stages of Alzheimer’s Disease2.  MEND is now in version 3.0, has been actively healing Alzheimer’s patients for nearly 5 years, and involves personalized solutions for a myriad of categories following identification of the etiology behind an individual’s diagnosis: with the cumulative result, that over 500 individuals who have gone through the MEND program (as Bredesen reported early this year) have not only stopped Alzheimer’s progression, but have reversed cognitive decline1,2,31

Part II: Epidemiology/etiology Molecular mechanism of the disease

One of the mentors of Dale E. Bredesen, PhD is Stanley Prusiner who received a Nobel Prize for his discovery of the prion, or mutant form of infectious protein found to be responsible for many neurodegenerative diseases including Creutzfelt-Jakob Disease1.  Prions are what is responsible screen-shot-2017-05-01-at-9-57-59-pmfor shifting of balance among proteins involved in synaptic reorganization (forgetting) and synaptic maintenance (remembering).  Bredesen argues that Alzheimer’s is a molecular cancer, where the amplification occurs at the biochemical (protein) level instead of the cellular level, which is possibly driven by prion replication and resultant imbalance31, 38

It was Bredesen’s group in 1993 that discovered “dependence receptors”, so named because they created states of dependence on their respective ligands23,31,39.  Bredesen’s group found that in vitro when they transfected any gene associated with neurodegeneration into neural cells, the probability that they commit suicide increases31.  Looking into the cause of this programmed cell death, Bredesen’s group found that dependence receptors induce the death of cells when they don’t get appropriate trophic support31.  Amyloid precursor protein (APP) that lies at the heart of Alzheimer’s Disease is one of these receptors31.  This is where Bredesen’s conception of a plasticity balance at the heart of the pathology arises2,42.  Depending on where APP is cleaved, it will either support neurite extension or neurite retraction2,42.  Two types of lesions in the brain characterize screen-shot-2017-05-01-at-1-53-57-pmAlzheimer’s: “extracellular senile plaques consisting primarily of amyloid precursor protein (APP)-derived amyloid-β (Aβ) peptide and intracellular neurofibrillary tangles consisting largely of hyper-phosphorylated microtubule-associated tau protein42.

Synapse loss and neuronal cell death represent the basis for cognitive impairment in AD, and the C-terminal caspase cleavage of APP resulting in release of a 31 amino acid C-terminal fragment has been shown to be a likely contributor to neuronal death in AD42.

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Amyloid-β (Aβ) peptide is the main component of Alzheimer’s Disease plaques and is derived from Amyloid Precursor Protein (APP).

Dr. Bredesen’s own research argues that amyloid is a protective response to three categories of threat; he explains that organisms make amyloid for three reasons31:

  1. Infection or Inflammation.  Senile plaques were actually found to consist of colonies of Spirochetes, bacteria commonly found in oral cavities which are associated with gum disease28.  See a video of them here:  https://www.youtube.com/watch?v=fy_C2XWzeXo  A-beta is a very good indigenous anti-biofilm28.  It binds metals with an ability comparable to ethylenediaminetetraacetic acid (EDTA) used in chelation therapy, & it is toxic to bacteria (antibiotic effect)28.
  2. Trophic withdraw.  Neurons from which Nerve Growth Factor (NGF) is withdrawn, will make beta amyloid protein as part of their programmatic downsizing process29.
  3. Toxic assault.  When bacteria is challenged with toxins, it makes amyloid as a protective response, with the ability to bind and sequester the toxins,28,30.

Dr. Bredesen believes that there are many different causes of Alzheimers and many routes for problematic substances to take to our brain31.  Diversity in non-pathologenic microbial communities at crucial sites on the body including oral, nasal, otic cavities, GI tract, skin and urogenital tracts is critical toward avoiding disease36.  Where Alzheimer’s is concerned, there are clear links with imbalance & inflammation in our oral microbiome, our sinonasal bacterial microbiome as well as gut microbiome.  The relationship between the health and diversity of our gut bacteria with our brain health and disease resistance was decisively established by a recent double-blind placebo controlled trial where just in 12 weeks, patients on probiotics were observed to have decreased levels of inflammatory marker hs-CRP by 18%, with a substantial improvement in brain function mini-mental status exam (MMSE) score, while patients not on probiotic therapy increased hs-CRP by 45% and experienced a huge reduction in brain function capability.34  “Decreased bacterial richness and diversity” in the sinonasal bacterial microbiome has been shown to have links to chronic disease35,36.  An estimated 500,000 of the 5.2 million Americans currently diagnosed with and suffering from Alzheimer’s disease symptoms actually may have Inhalational Alzheimer’s Disease (IAD), which is curable37.  Those patients tend to display lab biomarkers of Chronic Inflammatory Response Syndrome (CIRS) and fall under Dr. Bredesen’s Type3AD definition explained below37.  Oral inflammation is heavily associated with Alzheimer’s, notably that involving p.gingivalis, Oral Herpes Simplex Virus (HSV-1), or Spirochetes microorganisms31,46.  Periodontitis and gingivitis have both been linked to Alzheimer’s31,46.

Dr. Bredesen has put Alzheimer’s Disease patients in different groups according to their metabolic profiling data45:

Type 1AD:  Inflammatory (hot).  Includes sterile inflammation or infection-related inflammation.  Inflammation stimulates amyloid secretion.  External drivers & Internal drivers include sugars in our diet, high transfats – inflammatory processes31,45.

Type 1.5AD: Glycotoxic (sweet). Internal drivers of inflammation include insulin resistance (gives you the atrophic portion & type 2AD) & glycated proteins (cause the inflammation that gives you the type 1AD31,45.

Type 2AD: Atrophic (cold). Signs of trophic support withdraw, and amyloid is being produced as part of a programmatic downsizing. Patients observed to be deficient in trophic support biomarkers including Nerve Growth Factor, Brain Derived Neurotrophic Factor, estradiol, testosterone, thyroid hormone, vitD, vitB12, folate, estradiol, and have a high copper to low zinc ratio.  Other telltale biomarkers for this version of Alzheimer’s Disease indicate methylation defects, and high homocysteine.  Dr. Bredesen said they use the George Brewer protocol to correct zinc deficiency (zinc picolinate, small amount of Manganese, vitB6, N-Acetyl Cysteine, high dose of ascorbate)31,33,45.

Type 3AD: toxic (vile): external drivers of inflammation include chemical exposure (like pesticides and BPA), heavy metals (like mercury, lead, cadmium and arsenic),  and biotoxins (like mold spores, mycobacteria, fungi, endotoxins, inflammagens, and microbial volatile organic compounds).  Almost all Dr. Bredesen’s patients with the HLA-DRDQ haplotype are highly sensitive to biotoxins31.  Many different microorganisms are associated with Alzheimers, especially in biofilms (p.gingivalis, Oral Herpes Simplex Virus (HSV-1), Spirochetes, Borelia burgdorferi, etc)31,45.

Since the time Dr. Bredesen published his research paper on 3 types of Alzheimer’s, he has in lectures described 5 types, the last two being related to Type 2AD, and they are Type 4AD which is “vascular” (pale) with atherosclerotic/cardiac risk symptoms, and Type 5AD which is “traumatic” (dazed) with previous history of head trauma31,45.

Part III: Assessment of Risk Factors, and Nutritional Deficiencies of the Disease

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There are 60 different things measured in Dr. Bredesen’s MEND 3.0 protocol31.  He includes diagnostic testing of these variables as well as a functional medical assessment, and puts them in a computer algorithm to determine proper Alzheimer’s type and treatment31.  Here are a collection of the top indices mentioned by Dr. Bredesen collectively representing high risk for Alzheimers:

1.ApoE4 homozygous. 

ApoE4 is present in 95% of late-onset Alzheimer’s Disease cases, and as such is considered a screen-shot-2017-05-01-at-9-35-16-pmmajor genetic risk factor for Alzheimer’s Disease.1,40.  ApoE3 is the dominant gene worldwide, representing 75% of Americans, and this majority has a 9% risk of contracting Alzheimer’s1,31.  75 million Americans have 1 copy of ApoE4, and they have a 30% risk of contracting Alzheimer’s as a result1,31.  The unfortunate 7 million with 2 copies have a 90% chance1,31.

Interestingly, all Hominids were ApoE4 homozygous up until the discovery of fire.

Apolipoprotein E (ApoE) is a glycoprotein that consists of 299 amino acids, which is the major protein component of very low-density lipoproteins (VLDL) as well as the major apolipoprotein present in our brain26. ApoE assists in regulating cholesterol and lipid metabolism, as well as in cellular repair25.  The ApoE gene is positioned on chromosome 19, and has three isoforms, Apo2, 3, & 425.

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Plasticity Imbalance:  When a cell is in a ApoE4 dominant state, the cell turns on an inflammatory cascade that involves RelA (phosphorylation of which regulates NF-kappaB activation)27.  ApoE4 binds to 1700 genes in their promoter regions, many of which involve microtubule disassembly, glucose homeostasis, synaptic dysfunction, and inflammation.  If a cell is in an ApoE3 dominant state, the cell will put more resources into recycling and longevity.

Plasticity Imbalance:  Of the three isoforms, “only screen-shot-2017-05-01-at-1-52-47-pmApoE4 significantly reduces the ratio of soluble amyloid precursor protein alpha (sAPPa) to Amyloid beta, reduces Sirtuin T1 (SirT1) expression [up to 80%], resulting in markedly differing ratios of neuroprotective SirT1 to neurotoxic SirT2, triggers Tau phosphorylation (p-Tau) and APP phosphorylation ((p)-APP), and induces programmed cell death”24.  You may recall (I explained earlier in this report) that Alzheimer’s Disease “tangles” consist largely of hyper-phosphorylated tau protein.  You also may recall that amyloid-β (Aβ) peptide is the main component of Alzheimer’s Disease “plaques” and is derived from Amyloid Precursor Protein (APP).  All of these ratio shifts are favoring propensity for synaptoclastic activity instead of synaptoblastic activity.

2. Homocysteine greater than 7.  Elevated homocysteine levels and oxidative stress are directly linked to Alzheimer’s Disease risk20,21.

3. Vitamin B12 less than 5001,31.  Low B-vitamin intake is linked to Alzheimer’s risk17, 18.  Other vitamins and minerals Dr. Bredesen routinely measures low in Alzheimer’s patients include VitC, VitK2, folate, magnesium, and zinc31,44.  Vitamin D intake is especially critical, with blood levels under 30 linked to Alzheimer’s risk19.

4. hs-CRP greater than 1.01,31

5. Total Protein and Albumin/Globulin (A/G) ratio less than 1.81,31

6. Hemoglobin A1c (HbA1c) greater than 5.61,31

7. Fasting insulin greater than 6 uIU, and Fasting Blood Sugar greater than 901,31.  Dr. Bredesen remarks that “as metabolism goes, so goes the cognition”31.  Metabolic Syndrome, Type 2 Diabetes, and Prediabetes all carry greater risk for Alzheimer’s Disease1,31.

8. Simple carbs in diet.  Frequent simple carbohydrate ingestion has been linked to risk of Alzheimer’s6.

9. Thyroid: TSH greater than 2.0, Free T3 less than 3.2, Reverse T3 greater than 20, and Free T4 less than 1.3.1,31

10. Post-menopausal1,31

11. Sleep apnea or hypopnea.  Little (< 6 hours) or poor quality sleep is linked to Alzheimer’s31,41.

12. Low androgen levels: Total Testosterone (T) less than 500, and Free T less than 6.51,31.

13. Low estradiol: E2 less than 100, hysterectomy at under 41 years old1,31.

14. Low pregnenolone: under 201,31.

15. History of head trauma1,31.  Retired National Football League players are 4-times more likely to die of Alzheimer’s than the general US population43.

16. DHEA intake.  Low DHEA intake is solidly linked to Alzheimer’s risk7,9,10,11, 18

17. Cholesterol measured greater than 255 or less than 150 carries a greater risk for Alzheimer’s Disease1,31.

18.  Prescription & nonprescription drugs also notably raise Alzheimer’s risk, including:

    • Statins:  In 2011 a study was published coauthored by Dr. Bredesen, reviewing all the drugs the FDA had approved for their effects on Alzheimer’s, and the drugs that had the highest negative effect on Alzheimer’s progression were statin drugs13.   Statins and lipophilic statins like simvastatin and cerivastatin in particular were found to stimulate Abeta production42. Dr. Bredesen refers to statins as “dementegens”, and believes just like we currently name some substances “carcinogens” the same type labeling should arguably apply to warn of the increased risk for neurodegenerative disease31.
    • PPIs:  Beta-amyloid (Aß) plaque increases in the brains of mouse models when PPIs are used:  “Aß aggregation leads to formation of fibrillar b-pleated sheet structures that are major components of extracellular senile plaques which are found in the brains of AD patients”14  Acidic lysosomes located within phagocytic microglia play a critical role  in their digestion of fibrillar Aß (fAß)14.  When these lysosomes become less acidic, they can no longer degrade & clear fAß, a major step in the pathogenesis of Alzheimers14. Studies have shown that clearing fibrillar Alzheimer amyloid-ß peptide (fAß) is effective Treatment for Alzheimers, at least in murine models14.  PPIs suppress the secretion of gastric acid “by inhibition of the H+/K+ ATPase present on the plasma membrane of the gastric parietal cells”, but have been demonstrated by several studies to both penetrate the blood-brain barrier, and to block V-ATPases on macrophages’ lysosomal membrane14.  It is a reasonable hypothesis that PPIs also inhibit V-ATPases on microglia’s lysosomal membranes, lowering lysosome acidification and reducing fAß clearance14. Dr. Bredesen commented that when he sees an Alzheimer’s patient with a low zinc level, he usually asks them if they are on PPIs, and they usually are. 
    • Neuroactive medications have been solidly linked to Alzheimer’s disease risk15.
    • Illicit Drugs.  Use of illicit drugs has been linked to Alzheimer’s risk1,31.

Part IV: Interventions

Typical medical treatment for the disease:  

Conventional treatment for Alzheimer’s usually includes prescription of cholinesterase inhibitors (donepezil, rivastigmine and galantamine), or the NMDA antagonist memantinemedication.  Cholinesterase inhibitors (like often prescribed Donepezil (Aricept) HCL 5mg) prevents acetylcholine breakdown in brain tissue though its inhibition of cholinesterase, and is often used in treating dementia symptoms47.  But the prognosis is bleak:   out of 244 drugs approved for Alzheimers in the last decade, all but one have failed to treat the pathology, and the one that avoided abject failure has very minimal advantageous effects1.

Dr. Bredesen’s Nutritional & Lifestyle Management for Alzheimer’s Disease

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Intervention that has seen progress (even reversal of cognitive decline and regrowth of brain tissue) with Alzheimer’s patients is Dr. Bredesen’s 36-point MEND 3.0 personalized therapy program.  Dr. Bredesen describes his MEND 3.0 intervention as always starting with optimal Nutrition, and puts an emphasis on its involvement not only in the initial intervention, but in continued management of the disease1.  He directs patients to convert from high-carb diets to good-fat diets, and directs that all simple carbohydrate food-sources (highly-processed) should be completely cut out1.  His own and others’ empirical evidence shows these changes assist patients with managing their fasting insulin levels and regaining insulin sensitivity6,8,31.  Both the ketogenic diet and the real-food Mediterranean Diet have shown reduced risk of Alzheimer’s in research8,16.  Bredesen also administers food sensitivity/allergy testing to his patients in order to determine which foods cause them gut dysfunction, chronic inflammation, and impaired nutrient absorption1.  His participants are given prebiotics and probiotics to avoid inflammation and autoimmunity34.  Bredeson also uses targeted herbs shown to reduce inflammation and Abeta including curcumin and ashwagandha1,31.  He prescribes high-dose antioxidants like glutathione and vitC, cod liver oil for DHA/EPA, vitamin A, D, and additional K2 supplementation for healthy bones1,31.  Dr. Bredeson administers an Organic Acids Test to rule out CIRS, toxins, and infections including yeast or bacterial dysbiosis and to get an initial determination of metal homeostasis1,31.  He initiates adrenal support and hormone optimization for patients’ (usually) hypothyroid symptoms, and prescribes supplementation of nutrients such as 5-HTP, melatonin, and L-theanine to support participant’s sleep quality1,31,41.  He also looked for drugs that would help put his patients on the correct side of APP processing and found one called FO3 that is now currently in clinical trial in Australia31.

Part V:  Discussion

Dr. Bredesen describes Alzheimer’s as your roof having 36 holes in it.  His multifaceted therapy involves plugging as many holes as possible, whereas every single drug currently on trial for Alzheimers is a monotherapy drug1.  For such a a complex pathology with a variety of potential causes and presenting with a range of symptoms, is it any wonder that plugging one or two holes has little effect on Alzheimer’s progression?  Naturally a patient presenting with Type1AD-causes calls for vastly different therapeutic targets than one presenting with type3AD-causes.  The source of Alzheimer’s (& there are many!!) needs to be understood in order to stop the progression of neurodegenerative decline, and then needs to be addressed on an individualized basis using a multifaceted method.  This chronic disease like many others needs to be addressed through a Functional Medicine approach.  Being that this is currently the only viable approach, Alzheimer’s treatment could signal a paradigm shift in medical practice where Functional Medicine gets integrated into conventional medicine.  It is an amazing, exciting time to be a student of Human Nutrition!  We can prove with documented, objective, and peer-reviewed evidence that progressive memory loss has been reversed and disease markers have disappeared in a chronic, hopeless disease with no pharmaceutical solution.  These paradigms will hopefully serve as a wrecking ball to obliterate a conventional model which clings to pharmaceutical solutions being the only option when it comes to chronic disease. 

Resources

1. Bredesen, Dale E. (24 Feb 2016). Insights from Metagenics PreConference. Cognitive Health: Dawn of the Era of Treatable Alzheimer’s Disease. Integrative Healthcare Symposium Pre-Conference. Midtown, New York City

2. Bredesen, D. E., Amos, E. C., Canick, J., Ackerley, M., Raji, C., Fiala, M., & Ahdidan, J. (2016). Reversal of cognitive decline in Alzheimer’s disease. Aging (Albany NY), 8(6), 1250–1258. http://doi.org/10.18632/aging.100981  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4931830/

3. European Commission’s Scientific Committee on Consumer Safety (SCCS) Opinion On the safety of aluminium in cosmetic products (27 Mar 2014). http://ec.europa.eu/health/scientific_committees/consumer_safety/docs/sccs_o_153.pdf

4. Tomljenovic, Lucija. “Aluminum and Alzheimer’s disease: after a century of controversy, is there a plausible link?.” Journal of Alzheimer’s Disease 23.4 (2011): 567-598.  http://eds.a.ebscohost.com.libproxy.bridgeport.edu/ehost/pdfviewer/pdfviewer?sid=8fe45ed9-970d-4344-a028-060cbde1c3c5%40sessionmgr4007&vid=1&hid=4113

5. James, B. D., Leurgans, S. E., Hebert, L. E., Scherr, P. A., Yaffe, K., & Bennett, D. A. (2014). Contribution of Alzheimer disease to mortality in the United States. Neurology, 82(12), 1045–1050. http://doi.org/10.1212/WNL.0000000000000240

6. Tay, J., Zajac, I. T., Thompson, C. H., Luscombe-Marsh, N. D., Danthiir, V., Noakes, M., … & Brinkworth, G. D. (2016). A randomised-controlled trial of the effects of very low-carbohydrate and high-carbohydrate diets on cognitive performance in patients with type 2 diabetes. British Journal of Nutrition, 116(10), 1745-1753. https://www.cambridge.org/core/journals/british-journal-of-nutrition/article/div-classtitlea-randomised-controlled-trial-of-the-effects-of-very-low-carbohydrate-and-high-carbohydrate-diets-on-cognitive-performance-in-patients-with-type-2-diabetesdiv/761CC40CC2DECA7B2260B5912F4F9694

7. Belkouch, M., Hachem, M., Elgot, A., Van, A. L., Picq, M., Guichardant, M., … & Bernoud-Hubac, N. (2016). The pleiotropic effects of omega-3 docosahexaenoic acid on the hallmarks of Alzheimer’s disease. The Journal of Nutritional Biochemistry, 38, 1-11. http://www.sciencedirect.com.libproxy.bridgeport.edu/science/article/pii/S0955286316300225

8. Gasior, M., Rogawski, M. A., & Hartman, A. L. (2006). Neuroprotective and disease-modifying effects of the ketogenic diet. Behavioural Pharmacology, 17(5-6), 431–439. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2367001/

9. Bazan, N. G., Molina, M. F., & Gordon, W. C. (2011). Docosahexaenoic Acid Signalolipidomics in Nutrition: Significance in Aging, Neuroinflammation, Macular Degeneration, Alzheimer’s, and Other Neurodegenerative Diseases. Annual Review of Nutrition, 31, 321–351. http://doi.org/10.1146/annurev.nutr.012809.104635 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3406932/

10. Tremblay, M.-E., Zhang, I., Bisht, K., Savage, J. C., Lecours, C., Parent, M., … Maysinger, D. (2016). Remodeling of lipid bodies by docosahexaenoic acid in activated microglial cells. Journal of Neuroinflammation, 13, 116. http://doi.org/10.1186/s12974-016-0580-0.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4879742/

11. Esfahani, A., Somi, M. hossein, Ayromlou, H., Nikanfar, A., Jafarabadi, M. A., Sadat, B. E., & Ghoreishi, Z. (2016). The effect of n-3 polyunsaturated fatty acids on incidence and severity of oxaliplatin induced peripheral neuropathy: a randomized controlled trial. Biomarker Research, 4, 13. http://doi.org/10.1186/s40364-016-0066-3 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4918070/

12. Nehls, M. (2016). Unified theory of Alzheimer’s disease (UTAD): implications for prevention and curative therapy. Journal of Molecular Psychiatry, 4, 3. http://doi.org/10.1186/s40303-016-0018-8 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4947325/

13. Descamps, O., Zhang, Q., John, V., & Bredesen, D. E. (2011). Induction of the C-terminal proteolytic cleavage of AβPP by statins. Journal of Alzheimer’s disease: JAD, 25(1), 51. http://eds.b.ebscohost.com.libproxy.bridgeport.edu/ehost/detail/detail?sid=a55006a9-057b-49e2-b779-75acce60aa6f%40sessionmgr107&vid=0&hid=111&bdata=JnNpdGU9ZWhvc3QtbGl2ZSZzY29wZT1zaXRl#AN=61216288&db=aph

14. Fallahzadeh, M. K., Borhani Haghighi, A., & Namazi, M. R. (2010). Proton pump inhibitors: predisposers to Alzheimer disease?. Journal of clinical pharmacy and therapeutics, 35(2), 125-126.  https://www.researchgate.net/profile/Mohammad_Kazem_Fallahzadeh/publication/44586630_Proton_pump_inhibitors_predisposers_to_Alzheimer_disease/links/54353ccd0cf2bf1f1f283733.pdf

15. de Gage, S. B., Moride, Y., Ducruet, T., Kurth, T., Verdoux, H., Tournier, M., … & Bégaud, B. (2014). Benzodiazepine use and risk of Alzheimer’s disease: case-control study. Bmj, 349, g5205. http://www.bmj.com/content/349/bmj.g5205/

16. Pérez-López, F. R., Chedraui, P., Haya, J., & Cuadros, J. L. (2009). Effects of the Mediterranean diet on longevity and age-related morbid conditions. Maturitas, 64(2), 67-79. https://www.researchgate.net/profile/Javier_Haya/publication/26780149_Effects_of_the_Mediterranean_diet_on_longevity_and_age-related_morbid_conditions/links/00b49529cbdd851196000000.pdf

17. Douaud, G., Refsum, H., de Jager, C. A., Jacoby, R., Nichols, T. E., Smith, S. M., & Smith, A. D. (2013). Preventing Alzheimer’s disease-related gray matter atrophy by B-vitamin treatment. Proceedings of the National Academy of Sciences, 110(23), 9523-9528. http://www.pnas.org/content/110/23/9523.long

18. Smith, D., Refsum, H., Oulhaj, A., de Jager, C. A., & Jerneren, F. (2016). Beneficial Interactions Between B Vitamins and Omega-3 Fatty Acids in the Prevention of Brain Atrophy and of Cognitive Decline in Early Stage Alzheimer’s Disease. The FASEB Journal, 30(1 Supplement), 407-6. http://www.fasebj.org/content/30/1_Supplement/407.6.short

19. Pludowski, P., Holick, M. F., Pilz, S., Wagner, C. L., Hollis, B. W., Grant, W. B., … & Soni, M. (2013). Vitamin D effects on musculoskeletal health, immunity, autoimmunity, cardiovascular disease, cancer, fertility, pregnancy, dementia and mortality—a review of recent evidence. Autoimmunity reviews, 12(10), 976-989. https://www.researchgate.net/profile/Maya_Soni/publication/236093841_Vitamin_D_effects_on_musculoskeletal_health_immunity_autoimmunity_cardiovascular_disease_cancer_fertility_pregnancy_dementia_and_mortality-A_review_of_recent_evidence/links/02e7e51d2836a98e3b000000.pdf

20. Miwa, K., Okazaki, S., Yagita, Y., Sakaguchi, M., Mochizuki, H., & Kitagawa, K. (2015). Increased Total Homocysteine Levels Are Associated With the Risk of Dementia Independently of Cerebral Small-vessel Disease. Stroke, 46(Suppl 1), A224-A224. http://stroke.ahajournals.org/content/46/Suppl_1/A224.short

21. Cankurtaran, M., Yesil, Y., Kuyumcu, M. E., Oztürk, Z. A., Yavuz, B. B., Halil, M., … & Arıoğul, S. (2013). Altered levels of homocysteine and serum natural antioxidants links oxidative damage to Alzheimer’s disease. Journal of Alzheimer’s Disease, 33(4), 1051-1058. http://content.iospress.com/articles/journal-of-alzheimers-disease/jad121630
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23.  Zhong, N., Scearce-Levie, K., Ramaswamy, G., & Weisgraber, K. H. (2008). Apolipoprotein E4 domain interaction: synaptic and cognitive deficits in mice. Alzheimer’s & Dementia, 4(3), 179-192.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2647370/
24.  Theendakara, V., Patent, A., Libeu, C. A. P., Philpot, B., Flores, S., Descamps, O., … & John, V. (2013). Neuroprotective Sirtuin ratio reversed by ApoE4. Proceedings of the National Academy of Sciences110(45), 18303-18308.  http://www.jstor.org.libproxy.bridgeport.edu/stable/pdf/23754779.pdf 
25.  Raichlen, D. A., & Alexander, G. E. (2014). Exercise, APOE genotype, and the evolution of the human lifespan. Trends in neurosciences37(5), 247-255.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4066890/ 
26.  Puglielli, L., Tanzi, R. E., & Kovacs, D. M. (2003). Alzheimer’s disease: the cholesterol connection. Nature neuroscience6(4), 345-351.  http://eds.a.ebscohost.com.libproxy.bridgeport.edu/ehost/pdfviewer/pdfviewer?sid=002afb55-392b-4374-a279-4a4884efb503%40sessionmgr4006&vid=1&hid=4108
27.  Lawrence, T. (2009). The nuclear factor NF-κB pathway in inflammation. Cold Spring Harbor perspectives in biology1(6), a001651.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2882124/
28. Miklossy, J. (2016). Bacterial amyloid and DNA are important constituents of senile plaques: further evidence of the spirochetal and biofilm nature of senile plaques. Journal of Alzheimer’s Disease53(4), 1459-1473.  http://content.iospress.com/articles/journal-of-alzheimers-disease/jad160451
29.  Capsoni, S., & Cattaneo, A. (2006). On the molecular basis linking nerve growth factor (NGF) to Alzheimer’s disease. Cellular and molecular neurobiology26(4-6), 617-631.  https://link-springer-com.libproxy.bridgeport.edu/article/10.1007/s10571-006-9112-2   
30.  Kumar, D. K. V., Choi, S. H., Washicosky, K. J., Eimer, W. A., Tucker, S., Ghofrani, J., … & Moir, R. D. (2016). Amyloid-β peptide protects against microbial infection in mouse and worm models of Alzheimer’s disease. Science translational medicine, 8(340), 340ra72-340ra72.  https://www.researchgate.net/profile/Robert_Moir2/publication/303532914_Amyloid-_peptide_protects_against_microbial_infection_in_mouse_and_worm_models_of_Alzheimers_disease/links/57605a7d08ae2b8d20eb600c.pdf 
31. Bredesen, Dale E. “Reversing Alzheimer’s Disease” (17 Nov 2016) Silicon Valley Health Institute presentation. https://www.youtube.com/watch?v=6D5aA_-3Ip8
32. Theendakara, V., Peters-Libeu, C. A., Spilman, P., Poksay, K. S., Bredesen, D. E., & Rao, R. V. (2016). Direct transcriptional effects of apolipoprotein E. Journal of Neuroscience, 36(3), 685-700.  http://www.jneurosci.org/content/36/3/685.full

33. Brewer, G. J. (2016). Alzheimer’s disease causation by copper toxicity and treatment with zinc. Frontiers in aging neuroscience, 6.  http://journal.frontiersin.org/article/10.3389/fnagi.2014.00092/full

34. Akbari, E., Asemi, Z., Kakhaki, R. D., Bahmani, F., Kouchaki, E., Tamtaji, O. R., … & Salami, M. (2016). Effect of probiotic supplementation on cognitive function and metabolic status in Alzheimer’s disease: a randomized, double-blind and controlled trial. Frontiers in Aging Neuroscience, 8.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5105117/

35. Ramakrishnan, V. R., Hauser, L. J., & Frank, D. N. (2016). The sinonasal bacterial microbiome in health and disease. Current opinion in otolaryngology & head and neck surgery, 24(1), 20.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4751043/

36. Bhattacharjee, S., & Lukiw, W. J. (2013). Alzheimer’s disease and the microbiome.  http://journal.frontiersin.org/article/10.3389/fncel.2013.00153/full     

37. Bredesen, D. E. (2016). Inhalational Alzheimer’s disease: an unrecognized—and treatable—epidemic. Aging, 8(2), 304-313.  http://www.aging-us.com/article/100896/text

38. Goedert, M. (2015). Alzheimer’s and Parkinson’s diseases: The prion concept in relation to assembled Aβ, tau, and α-synuclein. Science, 349(6248), 1255555.  https://pdfs.semanticscholar.org/052d/df6970cbbc36bc74cf5daecfb3771e96bf46.pdf

39. Bredesen, Dale E (2016) Prionic Loops, Anti-Prions, and Dependence Receptors in Neurodegeneration Buck Institute for Research on Aging, Novato, California. https://www.mpicognition.com/wp-content/uploads/2016/02/BredesenChapterSBPbook.pdf

40. Theendakara, V., Peters-Libeu, C. A., Spilman, P., Poksay, K. S., Bredesen, D. E., & Rao, R. V. (2016). Direct transcriptional effects of apolipoprotein E. Journal of Neuroscience, 36(3), 685-700.  https://www.mpicognition.com/wp-content/uploads/2016/01/2016-J-Neuro-ApoE.pdf

41. Nesse, R. M., Finch, C. E., & Nunn, C. L. (2017). Does selection for short sleep duration explain human vulnerability to Alzheimer’s disease?. Evolution, Medicine, and Public Health, 2017(1), 39.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5381352/

42. Poksay, K. S., Sheffler, D. J., Spilman, P., Campagna, J., Jagodzinska, B., Descamps, O., … & Cosford, N. D. (2017). Screening for small molecule inhibitors of statin-induced APP C-terminal toxic fragment production. Frontiers in Pharmacology, 8.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5309220/
43. Lehman, E. J., Hein, M. J., Baron, S. L., & Gersic, C. M. (2012). Neurodegenerative causes of death among retired National Football League players. Neurology, 79(19), 1970-1974.  http://www.revdesportiva.pt/files/para_publicar/Neurodegenerative_causes_of_death_among_NFL_players.pdf 

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45. Bredesen, D. E. (2015). Metabolic profiling distinguishes three subtypes of Alzheimer’s disease. Aging (Albany NY), 7(8), 595-600. http://www.aging-us.com/article/100801/text

46.  Abbayya, K., Puthanakar, N. Y., Naduwinmani, S., & Chidambar, Y. S. (2015). Association between periodontitis and Alzheimer’s disease. North American journal of medical sciences, 7(6), 241  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4488989/

47. National Institute on Aging. National Institutes of Health. “Alzheimer’s” (2015) https://www.nia.nih.gov/alzheimers/topics/diagnosis

Zur Nutrition Challenge 2016:

Rückblick: In den Jahren 2012 bis 2014 lebte ich in Moskau und machte meine Erfahrungen mit dem russischen Winter  (+12kg).

 

Ich entschied mich mit CrossFit zu beginnen. Ehrlich, das änderte alles, denn gepaart mit Einkaufen am lokalen Gemüse- & Fleischmarkt und ‚frisch gekocht ist halb gewonnen’ purzelten die Kilos!

 

Meine Motivation bei der Challenge (30 Tage – Eat Clean) teilzunehmen ist einfach erklärt: ich wollte beweisen, dass PALEO funktioniert und, dass die Ernährungsweise bei weitem nicht so ungesund ist wie von vielen Ernährungsberatern- und Coaches postuliert. – Deswegen habe ich täglich Puls, Blutdruck und Gewicht gemessen.

 

Es versteht sich von selbst, dass je länger die Challenge dauerte sich meine Puls-, Blutdruck- und Gewichts-Werte wesentlich verbesserten und meine Leistungsfähigkeit massiv anstieg.

 

Am letzten Tag der Challenge hatte ich ein Gewicht von 60,5kg mit einem Blutdruck von 106/69 und einen Ruhepuls von 48S/min – und verbesserte damit beim Benchmark Workout meinen persönlichen Rekord um ganze 31 Sekunden.

 

Babs

About the Nutrition Challenge 2016:
Cross Fit changed my life since I started training in Jan 2014 in Moskau with Dmitry A. – who also knows Drake.
Everything since then seems to be connected.
As I told you – my first winter in Moscow was hard – I gained weight and was up at 77kg within 3 months – for a various of reasons.
Cross Fit and turning away from  triathlon long distance ”stress training” – combined with high glycemic carbohydrates – to ordinary cooking and visiting the local markets changed everything.
At this time I trained CF 2x a week, and prepared for my 70.3 in summer. At the time I feared that less volume would result in worse finish times – but ”HELL NO” – I ended up PB at the finish line with
only 8h – 10h of training load and this with no road km.
In 2014 we moved to Nürnberg – and had a first trial training at RCFN  and I must admit I was happily surprised 🙂 🙂
Not only that I immediately recognized the similarity in style – what Dmitry did in Moscow – and what Drake and Daniel and you Ginger are doing here at RCFN – I felt challenged and at home at the same time.
–  I liked that.
The Nutrition Challenge 2016:
My motivation behind the challenge actually was to prove my study materials and my lecturers at the IST Institut wrong AND of course Back YOU UP in  the same cause!
So I took measurements – of blood pressure, resting heart rate and weight every day (see enclosed in my file at the box).
Unsurprisingly I feel fitter and healthier than before – and I can happily say – you guys have earned my biggest smile 🙂
Thank you for your work and dedication!
Yours,
Babs
PS, I stuck to coffee – which was my only hope and drug during the challenge 😉

..                     vorher             nachher
Gewicht        59,5 kg            56,0 kg
Po                  38,5 inches     37,75 inches
Oberarm      9,75 inches     9,75 inches
Hals              13 inches         13 inches
Handgelenk   6 inches          6 inches
Ziele: gesunde Gewichtsreduktion trotz Stillzeit, weniger Stimmungsschwankungen und reinere Haut

Grundsätzlich muss ich sagen, dass ich mich seit Ende 2012 Paleo ernähre -mit strengen und weniger strengen Phasen. Von daher war die Challenge im Januar 2016 nicht meine erste, jedoch meine HÄRTESTE!

Speziell ist an dieser Challenge sicher meine Ausgangssituation: nach meiner Hochzeit, während meinen Flitterwochen, in meiner Schwangerschaft und Stillzeit habe ich mich immer häufiger der „80-20-Regel“ bedient. Diese „Ausnahmen“ habe ich in der letzten Challenge sehr stark zu spüren bekommen.

Ich bin zum ersten mal Mama geworden und hatte nicht nur mit Schwangerschaftsdiabetis zu kämpfen, sondern musste nach der Geburt mit starkem Haarausfall, Akne und überflüssiges Babyspeck leben, gepaart mit sehr wenig Schlaf, überfordernden Mami-Momenten und „Comfort Food“ ist das eine extrem ungünstige Mischung. Hinzu kommt, dass ich seid Tag 1 voll stille; man stolpert während Recherche zum Thema „Abnehmen in der Stillzeit“ immer wieder über die Aussage, dass Diät während der Stillzeit schlecht für Mutter und Kind sind, und daher stark davon abgeraten wird.

Warum auch eine gewöhnliche Diät machen, wenn ich die Vorzüge von Paleo schon erlebt habe und die positiven Effekte kannte!? Daher war klar, dass er nur eine Lösung für mich gab, mein Weg „back to the roots“, ich musste wieder Paleo essen, mich, meinen Darm und meine Einstellung zurücksetzen, weshalb mir die Challenge im Januar sehr(!) gelegen kam. Wieso ich überhaupt mit Paleo gebrochen habe ist mir unklar. Hätte ich doch wissen müssen, welchen Effekt eine „gewöhnliche” Ernährung mit Milchprodukten, Brot, Nudeln und Zucker auf mich hat.

Wenn ich vorher eine Challenge gemacht hatte, waren die ersten Tage aufregend. Ich habe jeden Tag auf den ominösen Zuckerentzug gewartet, gedacht dass es mich wie einen Hammer trifft und ich die Symptome kaum ertragen könnte. Ich muss zugeben, dass es in dieser Challenge so schlimm war wie noch nie. Die ersten sieben Tage waren extrem hart für mich. Ich hatte den(!) Zuckerentzug, vor dem ich mich die letzten Male immer gefürchtet habe. Kopfschmerzen, Heißhunger, Müdigkeit und dennoch Schlaflosigkeit, innerer Unruhe und Stimmungsschwankungen, vielleicht sogar Depression -kann man das so sagen!?- waren an der Tagesordnung. Ich musste mich wirklich zusammen reißen, mich meiner Herausforderung zu stellen und nicht schon in den ersten Tagen abzubrechen. Erschwerend kam mein Alltag als Mama mit Säugling hinzu. In den ersten Tagen zählte für mich nicht „das große Ganze“, sondern lediglich der Kampf von Mahlzeit zu Mahlzeit.

Mein Erfolgsrezept für diese Challenge: Wochenplan, Wocheneinkauf und Vorkochen!

Jede Woche haben mein Mann und ich einen Wochenplan für unsere Familie erstellt. So waren unsere Gerichte für Frühstück, Mittag- und Abendessen koordiniert und man musste bei großem Hunger nicht erst „kreativ werden“. Die an den Abenden gekochten Gerichte gab es aufgewärmt am nächsten Mittag. Zeitmanagement ist mit Kind sowieso das A und O.

Ich hatte zwischenzeitlich wieder Tiefs in der Challenge mit schlechter Laune und Überdruss. Wäre ich keine Mama würde ich sagen: schlaf einfach mal ne runde länger, das hebt die Laune 😉 Das kann man allerdings mit Bewegung an der Luft und wechselnden Rezepten ebenfalls gut überwinden. Sport stand für mich bei dieser Challenge nicht im Fokus. Mir ging es darum, mich buchstäblich wieder gut in meiner Haut zu fühlen, schade dass ich keine Bilder von meiner Haut gemacht habe. Dort war der vorher-nachher Vergleich wirklich enorm, was einen großen Einfluss auf mein Selbstbewusstsein hat. Darüber hinaus gab es weitere positive Effekte: Gewichtsreduktion, verbesserter Darmhaushalt und gute Laune. Der Grundstein für einen bewussteren Lifestyle ist gelegt und den letzten Pfunden der Kampf angesagt. Letztlich fühle ich mich nach der Challenge physisch als auch mental besser. Ich würde sogar sagen, dass ich glücklicher bin.

An dieser Stelle möchte ich mich ganz HERZLICH bei Ginger für ihren täglichen Support bedanken. Es ist viel einfacher eine solche Herausforderung durchzustehen, wenn man einen solchen Mentor an seiner Seite weiß! Danke.

In deutsch:

Seit mehreren Jahren mache ich nun schon dasselbe Spiel. In der ersten Jahreshälfte baue ich die unnötigen Kilos ab und bringe meinen Körper bis Ende des Frühjahrs in Wettkampfform; und in der 2. Jahreshälfte ernte ich die Früchte des Erfolgs und baue leider die unnötige Masse wieder auf ;-(

 

Daher war ich zu Beginn der Paleo-Challenge durchaus zuversichtlich, dass der gewünschte Effekt eintreten wird. Was dann aber durch diese konsequente Paleo-Ernährungsweise, und nochmals präzisiert durch die verschärften, aber plausiblen, Richtlinien der RCFN-Nutrition-Challenge, passierte, hat mich doch ziemlich erstaunt. Noch nie habe ich zuvor in so kurzer Zeit (30 Tage) mit sehr mässigem Sport (2x die Woche Crossfit und eine weitere Ausdauereinheit) so viele Kilogramm reduziert (-5kg), und gleichzeitig aber mein Fitness- & Energieniveau gesteigert: Baseline-Workout um 40s verbessert.

 

Ich kann nur sagen – Paleo-Ernährung funktioniert, selbst wenn man viel beruflich unterwegs ist wie ich. Ok, ich muss zugeben, dass ich nicht immer im Detail wusste mit welchem Fett/Öl vor Ort im Restaurant gekocht wurde JJJ, aber alleine schon meine gezielte Auswahl und Zusammensetzung der Speisen, in Verbindung mit Weglassen von Alkohol und einem vernünftigen Schlafverhalten (im Durchschnitt von 6h auf 8h gesteigert) habe ich einen für mich bahnbrechenden Erfolg erzielt!

 

Und das Bierchen, welches ich mir am Tag nach Ende der Challenge gegönnt habe (allerdings alkoholfrei), hatte einen überraschend langweiligen Geschmack … Hmm warum habe ich das früher als erfrischend empfunden …???

 

Im Lebensmittelgeschäft benötige ich allerdings nun 15min länger, da ich mich jetzt regelmässig über die unnützen Zutaten laut Verpackungstexten wundere, und in der Gemüseecke die Vielfalt respektiere. Ehrlich gesagt, vor 30 Tagen wusste ich noch nicht mal wie Sellerie, Fenchel, Avocado & Co aussehen … jetzt habe ich schon mal die Qual der Wahl … das Leben wurde damit komplizierter, aber auf jeden Fall spannender und geschmackvoller. Ich für meinen Teil werde diese Ernährungsreise weiterführen – weil ich erkannt habe, dass ich damit nachhaltig meine Lebensqualität verbessern kann, ohne insgesamt mehr Geld auszugeben (denn was ich an einem Mehr an Qualität investiere, spare ich mir durch Weglassen von unnützen Zutaten) – ich wundere mich auch regelmässig wer denn diese Vielzahl an ungesunden Nahrungsmitteln im Supermarkt überhaupt benötigt?

 

 

 

in english:

For a couple of years I’ve been following the same pattern. In the first half of every year I reduce unneccessary weight and push my body in shape for the upcoming sports competitions until the end of spring. In the second half of the year I usually harvest the fruits of success and try to enjoy life ;-(

 

For this reason, at the beginning oft the Paleo-Challenge I was quite confident that this method will work. But – it was really astonishing, which results a consequent Paleo-nutrition-behavior, additionally focused by the more precise RCFN-Nutrition-Challenge rules, had. Never in my life I‘ve lost so much weight (-5kg) in such a short time (30 days) while at the same time increasing my fitness- and energy-levels: my baseline WOD improved by 40sec, with only light sport activity (two times a week Crossift and one additional endurance exercise).

 

I can tell you: Paleo-Nutrition works! Even when you are travelling a lot. Ok, I have to admit, that I was not always sure which type of grease/oil was used for cooking at restaurants JJJ, but starting with an individual selection of foods and ingredients, combined with no consumption of alcohol and a reasonable sleep behavior (average increased from 6h to 8h) I achieved an outstanding victory for myself!

And the first beer (non-alcoholic), which I enjoyed after the end of the challenge, had a very lazy taste …!  Hmm, I was wondering why this tasted so colourful some weeks ago …???

 

In the supermarket I now need 15 minutes longer for shopping, because I wonder about unnecessary ingredients of normal foods. In the grocery corner I fully enjoy the variety of vegetables and fruits. Frankly speaking, 30 days ago I not even recognised celery, fennel, avocado & co … and now I have the challenge of abundance… My life got more complicated, but in any case more thrilling and definitely healthier. My decision is to continue this nutrion-journey – because I realized it is a reasonable way to boost quality of life without spending more money (the amount which I invest more in food quality, I will save with neglection of unnecessary food ingredients). – And I am really wondering who the ‚….‘  needs those huge amount of unhealty food stuff in the supermarkets anyways?

Der Kampf gegen Muffin Top – Ein Jahr und eine Challenge in der Retrospektive

 

Ich möchte über meine 30Tage schreiben, indem ich sie in einem größeren Kontext darstelle. In meinem Fall war das kein isoliertes Projekt, sondern ein Teil eines größeren Prozesses meine Art zu leben von Grund auf umzustellen. Die Challenge bedeutete für mich mehr als nur ein paar Kilo abzunehmen und Körperfett zu reduzieren. Es war der Beitrag zu meiner Zufriedenheit und Gesundheit, an dem ich interessiert war.

 

Noch vor einem Jahr war ich unzufrieden mit einem Körper. Ich gebe ganz offen zu, dass das der Grund war, warum ich mit CrossFit anfing. Nachdem ich einige Zeit im Fitnessstudio trainiert hatte, konnte ich keine Veränderung an meiner Fitness oder meinem Aussehen feststellen. Das lag nicht daran, dass ich irgendwelche Bewegungen falsch ausführte oder so. Es war einfach frustrierend nach einer Weile und machte auch keinen Spaß, sich zu fühlen wie in ein Hamster auf depperten Maschinen, die Kalorien direkt vor deinen Augen zählen, während du Fashion Shows auf ca. 15 Bildschirmen um dich herum anschauen musst (was für eine gemeine Idee). Eine Stunde fühlt sich wie ein ganzes Leben auf den Dingern an. Nachdem ich mich bei Reebok CrossFit Nürnberg angemeldet hatte, hat es nicht mehr als 2-3 Monate gedauert, bis ich die ersten 3 Kilo abgenommen hatte. Das funktionierte, ohne dass ich irgendetwas an meiner Ernährung verändert hatte. Ungefähr im Juni letzten Jahres beschloss ich, Paleo auszuprobieren und nahm ein paar weitere Kilos ab. Die Sache war die, dass ich zunächst nur aufhörte Brot, Nudeln, Reis und alles mit Gluten oder Getreide zu essen. Ich wusste, dass ich auf lange Sicht auch den Krieg gegen Zucker aufnehmen musste, aber für den Anfang habe ich mich für die Schlacht gegen Gluten und Kohlenhydrate aus Getreide entschieden. Im Oktober hörte ich erfolgreich auf zu rauchen. Die Challenge war eine Chance für mich, Unterstützung zu haben einen weiteren Schritt zu Machen und Milch und Zucker loszuwerden

 

Es funktionierte. Ich habe gegen den Blerch gewonnen. Ich möchte die 30 Tage nicht nur danach bewerten zu fragen Wie viel Kilo habe ich abgenommen? Es waren nicht viele. Die Challenge hat mich in einen Essensrhythmus gebracht. Das ist etwas, was ich aus dieser Zeit mitnehme. Für mich waren es 30 Tage ein Model zu etablieren für die Zeit nach der Challenge. Ich durchlebte alle Phasen: Ich war müde am Anfang, ich hatte Kopfschmerzen, ich war sauer, weil alle abnahmen außer mir, ich war wieder müde, ich hatte Blähungen, ich fragte mich, warum ich das eigentlich machte. Da realisierte ich erst wirklich, warum ich das machte (in Woche drei oder so): Ich wollte eigentlich nicht abnehmen, weil ich schon genug abgenommen hatte vor der Challenge. Ich wollte mich besser fühlen. Ich wollte ausgeglichener sein, um in den WODs besser zu werden. Aber für eine lange Zeit der 30 Tage, sagen wir bis irgendwann letzte Woche, also eine Woche vor Ende der Challenge, konnte ich nicht sehen, dass das eintritt. Mein Körper fühlte sich nicht richtig an. Ich fühlte mich nicht wohl. Das Gefühl, in diesem gesund essenden Köper zu stecken, hatte nichts mit der romantischen Idee eat-cleanfeel-nice Idee zu tun. Das war der Punkt, an dem ich dachte: F*** this sh**, Ich kehre zurück zu meinem milchigen Leben, wo Essen süß ist und man Hüften Hüften sein lässt. Meine langweilige Ges- 16.02.2016 chichte könnte hier enden. Ihr Armen. Ihr müsst noch ein wenig weiterlesen. Ich habe meinem Zorn und meiner Frustration nicht nachgegeben. Wenn ich daran dachte, aufzugeben, fing ich an, zu lessen. Ich versuchte, Erklärungen dafür zu finden, warum ich mich so fühlte oder wo meine Essensgelüste herkamen. Das musste mein Gehirn meinem Darm dann ernsthaft erklären. Die Facebook Gruppe und all das wissenschaftliche Lesematerial, das uns an die Hand gegeben wurde, war sehr hilfreich, um Einsicht zu gewinnen, was wir da eigentlich durchlaufen, wenn wir uns mit dem Bedürfnis nach Zucker auseinandersetzen. Nach den härtesten paar Tagen letzte Woche bin ich so froh, dass ich nicht aufgehört habe. Seit dem bin ich darüber hinweg. Mein Körper fühlt sich besser an denn je und ich habe keine Symptome mehr, die irgendwie mit dem Magen in Verbindung gebracht werden könnten. Ich kann glücklich behaupten, dass ich nie zuvor so im Gleichgewicht mit meinen Organen war. TMI? Sorry. Die 30 Tage waren meinem letzten Jahr CrossFit sehr ähnlich. Ich kam, um meinen Körper zu verändern und warf das schnell über Bord, um neue Ziele zu finden, die viel mehr Spaß machen. Als ich mit CrossFit angefangen hatte wechselte mein Ziel von Gewichtsreduktion auf Steigerung des Gewichts, das ich heben oder bewegen kann, und besser zu performen (und…und…und…). Ich vergaß, warum ich ursprünglich damit anfing. Und das ist gut so. Weil zur Hölle mit visueller Besessenheit. Ich hab die Perspektive auf Frauen, die durch Medien suggeriert wird abgelegt. Mit der Challenge verlief es ähnlich. Ich kam, um meine Ernährung für eine Weile umzustellen, und dachte eigentlich, dass ich danach wieder zu meiner Ernährungsroutine zurückkehre. Ich verlasse die Challenge mit dem Ziel, meine Ernährung auf lange Sicht so beizubehalten. Nebenbei bemerkt: Seit der Challenge erholt sich mein Knie sehr gut, doch es wäre wohl schwierig, da aus wissenschaftlicher Sicht Kausalität nachzuweisen, denke ich. Trotzdem möchte ich das gern erwähnen, weil ich daran glauben möchte, dass es sich hier um eine mögliche positive Konsequenz aus der Ernährungsumstellung handeln kann. Außerdem haben sich meine Beschwerden im unteren Rücken verbessert. Ich erhole mich schneller. Muskelkater im unteren Rücken löst nicht mehr meine üblichen Verspannungen aus. Meine Muskeln scheinen sich schneller wieder zu entspannen und zu erholen, sogar nach WODs, nach denen es normalerweise Wochen dauert, bis mein Rücken Verspannungen löst. Ich hab auch die ersten Toes-to-Bar letzte Woche geschafft und hatte eine Nah-Strickt-Pullup-Erfahrung direkt vor der durch das heutige WOD verursachten Nahtoderfahrung. Das scheint wohl Hand in Hand zu gehen. Diese Verbesserungen: Zufall? Vielleicht. Ich schreibe das hier absichtlich vor Baseline und Messen. Ich möchte davon schreiben, wie man sich am Ende der Challenge fühlt, ohne es an Zahlen festmachen zu wollen. Ich weiß, das werde ich nämlich tun, sobald das Messen und Baseline stattgefunden hat.

 

Ich habe die Challenge mit CrossFit in Bezug gesetzt, weil es keine Ernährungs-Challenge für mich gäbe, wenn nicht für das große CrossFit-Gesamtbild. Das morgendliche Workout wurde zu einem grundlegenden Antrieb in meinem Leben. Ich könnte mit Leichtigkeit einen Essay nur darüber schreiben. Ich verschone euch aber vor noch ein paar mehr Seiten. Stattdessen möchte ich Ihnen, Ginger Sladky, dafür danken, dass Sie das hier in Ihrer Freizeit für uns organisiert haben. Die Motivation, die Sie in die Challenge gebracht haben, ist einzigartig. Ich kann sehen, wie viel Stunden Arbeit und Ge- 16.02.2016 danken man investiert, um zu verändern, wie Menschen über etwas denken. Ich würde mir wünschen, dass Sie meine Geschichte vom persönlichen Kampf gegen das Muffintop (saulustiges, dass Sie das Wort benutzten) als Ihren Erfolg verbuchen, meine Denkweise über Essen zu verändern. Ich hoffe es motiviert Sie, dass es noch viele Ohren gibt, die nicht taub sind. Und weil ich schon so viel über das letzte Jahr CrossFit sagte, möchte ich meinen Bericht mit ein paar Worten über unsere Box schließen. Danke Drake Sladky und Daniel Voros und natürlich den anderen Coaches dafür, wie Ihr CrossFit formt, dafür wie ihr eure Erfahrung und euer Wissen vermittelt und dafür, dass Ihr jeden einzelnen von uns tagein tagaus individuell fordert. Es ist ein wunderschöner Ort den Ihr da erschaffen habt. An alle anderen Challenge Kämpfer: Danke für die Rezepte und Inspiration.

 

-Anonymous

PS.: Challenge Geständnisse: Manchmal aß ich mehr als eine Handvoll Cashews. Und manchmal, da bin ich mir sicher, dass der Berg von Nüssen auf meiner Hand nicht als eine Handvoll Nüsse mehr zählte. Aber die Berge wurden kleiner im Verlauf der Challenge. Ich bin kein Nüsse-Junkie mehr.

PPS: 23.02.2015: Meine Baseline Zeit hat sich von 5:42 auf 5:05 verbessert. Die Zahlen sind stimmen mit dem Gefühl der Verbesserung also überein 🙂

 

_____________________________________

 

The Struggle against the Muffin Top – One Year and One Challenge in Retrospective

 

I would like to write about the 30 day challenge by putting it into perspective. In my case, it wasn’t an isolated project but ties in with an ongoing process to change my way of living from scratch. The challenge meant more to me than just losing a couple of pounds and reducing body fat. It’s the contribution to my happiness and health that I was interested in.

 

One year ago I was unhappy with my body. I openly admit that that was the reason why I started CrossFit. Having worked out at the gym for quite some time, I couldn’t see any changes in fitness or looks. It’s not that I was executing movements wrong or anything. It was just frustrating after a while and it was no fun feeling like a hamster, being on silly machines that count calories right in front of your eyes, while you have to watch fashion shows on like 15 screens around you (what a cruel idea). An hour can feel like a lifetime on those things. After I had registered with Reebok CrossFit Nürnberg it didn’t take more than 2-3 months to lose the first 3 kilos. That was without changing anything about my diet. If anything I did eat more than before. Around June last year I decided to try paleo and lost another couple of kilos during the rest of the year. The thing is, I had only stopped eating bread and pasta and rice and anything that contains gluten or wheat at first. I knew that eventually I was going to have to take on the war on sugar too, but for starters I decided to fight the first war against gluten and carbs. In October I successfully quitted smoking. The challenge was my chance to get some support to take another step and get rid of milk and sugar.

 

It worked. I did beat the blerch. I don’t want to only asses the 30 days in terms of how many kilos did I lose? It weren’t many. The challenge got me into a rhythm of eating. That’s something I take from the challenge. To me it was 30 days to set the model for the time after the challenge. I went through all the stages: I was tired at first; I had headaches; I was angry, cause everybody else was losing weight but me; I was tired again; I was constipated; I was asking myself why I am doing this. That’s when I actually realized why I was doing this (week three or so): I didn’t even want to lose weight, because I had already lost enough pounds before the challenge. I wanted to feel better. I wanted to feel balanced in order to perform better in WODs. However, during a long time of these 30 days, say until last week sometime, so one week before the end, I couldn’t see that happening. My body felt wrong. I didn’t feel comfortable. The feeling being inside the healthily eating body had nothing to do with the romantic eat-clean-feel-nice idea. That was the point where I thought: F*** this sh**, I’m going back to the milky life, where food is sweet and hips are hips. My boring story could end right here. Unlucky you. You gonna have to read a little more. I didn’t give in to my anger and frustration. When I had the thoughts of giving up I started reading. I tried to find an explanation for why I felt this way or where my cravings came from and my brain needed to seriously explain that to my guts. The Facebook group and all the scientific reading material that was provided to us were so helpful to gain insight into what all of us were going through struggling with the need for sugar. After the hardest couple of days last week I am so glad I didn’t drop out. Since then I’m over it. My body feels better 16.02.2016 than ever and I am not feeling any of the symptoms that can be connected to unhappy guts. I can happily state that I have never felt so in balance with my guts ever. TMI? Sorry. The 30 days challenge was a lot like my last year of CrossFit. I came in to change my body and ended up throwing that overboard and pick a new goal which is more fun. When I started CrossFit my goals quickly changed from wanting to lose weight to wanting to be able to lift or move more weight, to perform better (and…, and,…, and…). I forgot what I actually came for. And that is good. Because to hell with visual obsession. I got rid of the media gaze on women. Same with the challenge. I came to optimize my diet for a while and planned to go back to my eating routine after that. I’m leaving with the goal to change my diet for good. On a side note, since the challenge my knee has been recovering well, but it would be hard to scientifically proof causality I guess. I would like to mention it though, because I just like to think that it is possible those positive effects are somewhat results of the change in nutrition. Furthermore, my lower back issues have improved. I recover faster. The sore muscles in my lower back don’t cause the usual tension anymore. They seem to be able to relax and recover, even after workouts where it usually takes weeks for my back to let go of that tension and to recover. I also accomplished the first toes-to-bar last week, and I had a near-strict-pullup experience right before the WOD gave me my near-death experience this morning. Seems to go hand in hand. These improvements: Coincidence? Maybe. I am purposely writing this before I do baseline again, also before the measuring. I want to report the feeling at the end of the challenge without relating it to numbers. I know I will do that as soon as the measuring and baseline will be done.

 

I related the whole challenge to the framework of CrossFit because there wouldn’t be a challenge for me if it wasn’t for the bigger CrossFit picture. The workout every morning has become a crucial motor in my life. I could easily write an essay about that. I will spare you another couple of pages though. Instead I would like to thank you, Ginger Sladky, for doing this in your free time. The spirit you brought to this project is one of a kind. I can see the many hours it takes and many thoughts that go into trying to change the way people think about something. I would like you to read my story about my personal struggle against the muffin top (so funny that you used that word btw) as your succeeding to change the way I think about food. I hope that it motivates you that there are a lot of ears which aren’t deaf. Since I said a lot about my last year with CrossFit I would like to close my report of the challenge with some words about our box. Thank you Drake Sladky and Daniel Voros and of course all the other coaches for the way you shape CrossFit, for the way you convey your expertise and for the constant and consistent challenging of each and every one of us. It’s a beautiful place you people have created. To all the other challenge fighters: Thanks for all the recipes and inspiration.

-Anonymous

PS.: Challenge confession: Sometimes I had more than a handful of cashews. And sometimes I am sure that the mountain of nuts on my hand couldn’t have passed as a handful of nuts. But the mountains got smaller during the course of the challenge. I am not a nut junkie anymore.

PPS: 23.02.2015: I improved my Baseline time from 5:42 to 5:05. So numbers fit my feeling 🙂

 

featured photo credit: http://favim.com/image/1940410/ 

Meine Bilanz nach strikten 30 Tagen Paleo Challenge:

Körpergewicht runter, von 80,5 kg auf 77,9 kg
Körperfettanteil runter, von 12,9% auf 12,3%
Halsumfang runter, von 14,5 inches auf 14,25 inches
Bauchumfang runter, von 35 inches auf 34 inches
Das für mich wohl wichtigste Ziel – Baseline Zeit verbessert, von 05:03 min auf 04:43 min (https://www.youtube.com/watch?v=kriqEYqNKL8)

Die diesjährige Paleo Challenge war für mich die insgesamt dritte in den letzten vier Jahren. Die erste war natürlich erfahrungsgemäß die schwierigste, denn zum ersten mal habe ich mich mit meiner Ernährung auseinander setzen müssen, und auch die Chance genutzt, Paleo nicht als Diät sondern als Ernährungsumstellung zu sehen. Damals verlor ich ungefähr 10 kg doch meine sportliche Leistung hat sich nicht wirklich verbessert. Was ich erstmal auch nicht so schlimm fand. Ich habe meine Ernährung nach den strikten Tagen auf ein 80/20 Prinzip umgestellt und seitdem größtenteils bewusst auf meine Ernährung geachtet (80%). Die restlichen 20% nutzte ich dann um ebenfalls bewusst cheaten zu können. Die zweite Challenge 2014 habe ich leider mit Hochzeitsvorbereitungen und anderen Ausreden etwas schleifen lassen und so kann man diese Zeit gar nicht richtig mitzählen.

Das Jahr 2015 war für mich mit der Geburt meines Sohnes, einem Hauskauf und anschließender Renovierung ein ereignisreiches Jahr. An eine gesunde Ernährung war aus zeitlichen und organisatorischen Gründen einfach nicht zu denken. Dann kam natürlich noch abschließend Weihnachten hinzu und so fiel die Entscheidung für eine erneute Teilnahme an einer strikten Paleo Nutrition Challenge 2016 nicht schwer. Doch diesmal sollte für mich eher meine sportliche Leistungssteigerung bei gleichbleibenden Körpergewicht im Vordergrund stehen.

Was meiner Frau und mir diesmal und zum ersten mal richtig geholfen hat, waren unsere wöchentlichen Ernährungspläne. Nach diesen Plänen haben wir eingekauft, keine Lebensmittel mehr verderben lassen und zum ersten mal auch erfolgreich größere Portionen für den nächsten Tag vorkochen können. Erst bei dieser dritten Challenge konnte ich ausreichend Nahrung zu mir nehmen, (fast) immer satt sein und daher den Heißhunger erfolgreich unterbinden.

screen-shot-2017-01-11-at-10-40-09-am
Ich kann jedem Menschen, egal mit welchen Ausgangsgewicht, sportlicher Verfassung oder Statur diese Form der Ernährung nur ans Herz legen. Vor allem aber die ersten strikten 30 Tage. Sind wir mal ehrlich, wer es nicht selbst probiert hat (ja, es sind nur 30 Tage, stell dich nicht so an!) kann auch und sollte auch absolut nicht mitreden. Die Vorteile während und am Ende der 30 Tage überwiegen jegliche Nachteile, Vorurteile, Gewohnheiten die man glaubt zu kennen.
Ich kann aus eigener Erfahrung versichern: absolut jeder Mensch wird bei dieser Ernährungsumstellung (nein, keine Diät mit JoJo Effekt) etwas positives für sich gewinnen. Also, warum es nicht einfach mal probieren und neugierig sein?
Mein Dank geht an Daniel für die Organisation und an Ginger, mit ihrer unermüdlichen Art, jeder noch so kleinen Unklarheit immer Rede und Antwort zu stehen. Noch in der ersten Challenge hat Sie uns eine Präsentation und Einführung zum Thema Paleo gegeben und dabei ist mir ein Zitat im Kopf hängen geblieben, welches sich nun für mich bewahrheitet hat:
“If you are training [CrossFit], you’ve only got one oar in the water if you aren’t talking about nutrition.” – Greg Glassman, 2010

Paleo – 30 Tage Challenge und mehr

 

Bevor ich die Paleo-Challenge über 30 Tage startete, habe ich mich bereits seit einiger Zeit nach Paleo-Regeln ernährt. Angefangen hat es vor ca. drei Jahren. Zunächst habe ich immer mehr Getreide minimiert oder weggelassen, aß gesund und griff kaum zu „künstlichen“ Lebensmitteln. Regelmäßiger Sport war auch immer ein Thema. Allerdings war ich eine richtige Naschkatze und konnte kaum auf Süßigkeiten wie Gummibärchen oder Schokolade verzichten. Auch Bier oder Wein gehörte dazu, genauso wie Cola light. Viele würden sagen, es sei ganz normal und gesund.

 

Als ich vor etwas über zwei Jahren mit Crossfit begann, war meine Ernährung ok, aber noch nicht ganz paleo. Körperlich war ich fit und weit von Übergewicht entfernt. Trotzdem wollte ich mehr und das „Weiche“ um den Bauch weg haben. Mein Problem war meine Arbeitssituation. Ich arbeite in der Weiterbildung und zu unserem Service gehört die Verpflegung der Seminarteilnehmer. Das Problem: Es steht überall (!!!) Essen – von belegten Brötchen, über Müsli, bis hin zu Kuchen und Keksen, sogar Eis. Ich hatte es irgendwann satt, permanent durchs Training Center zu schleichen und hier und da was mitzunehmen, um es dann am Schreibtisch zu essen.

 

Je mehr ich über Paleo las, desto neugieriger wurde ich es auszuprobieren. Denn im Vergleich zu anderen Ernährungsvorgaben oder Ratschlägen macht Paleo für mich Sinn. Ich finde Paleo schafft eine natürliche Balance. Eine Waage ist überflüssig. Mein Entschluss war gefasst: Ich will auf Industrie-Lebensmittel, bei denen noch ein Food-Designer seine Finger im Spiel hatte, verzichten. Für mich heißt das alles oder nichts. Denn wenn ich einmal anfange zu mogeln, dann ist das zweite und dritte mal Mogeln auch nicht weit und der Paleo-Lifestyle ist dahin. Von nun an also kein Getreide, kein Reis, keine Milchprodukte und keine Süßigkeiten mehr – und das ohne zu mogeln oder einen Cheat-Tag einzulegen. Glücklicherweise ging es meinem Mann ähnlich und so funktionierte die Umstellung zu Hause problemlos (er gönnt sich allerdings immer mal wieder was, das nicht paleo entspricht).

 

Ich bin froh, dass ich kein Kuchen-Junkie und Brot-Verfechter bin. Daher fiel es mir bei manchen Dingen nicht schwer. Mein Frühstück besteht seit mehreren Jahren aus Rührei mit den unterschiedlichsten Gemüsevarianten. Und da der Entschluss gefasst wurde Paleo bestmöglich umzusetzen, gab es eben keine Süßigkeiten mehr. Nix, aus, vorbei! Ich fragte zwar nicht im Restaurant, welche Öle zum Braten genutzt werden, aber zu Hause achtete ich sehr darauf. Und in der Arbeit? Das Essen mit den Seminarteilnehmer war immer möglich: Gemüse oder Salat mit Fleisch fand ich immer. Und statt zum Süßkram zu greifen, plünderte ich von nun an die Obstschalen und die Nüsse. Ich war sehr erstaunt, wie gut und schnell man sich daran gewöhnt.

 

Ein paar wenige nicht Paleo konforme Lebensmittel blieben noch: Ab und zu ein Glas Wein war für mich ok und auf Elisen-Lebkuchen in der Weihnachtszeit wollte/ will ich auch nicht verzichten, die sind ohnehin getreidefrei. Auch Butter ist für mich ok, v.a. weil ich Bulletproof-Coffee für mich entdeckt habe.

 

Auch in der Schwangerschaft habe ich meine Paleo-Ernährung beibehalten, abgesehen von wenigen Ausnahmen (ich erinnere mich an zwei Wochen oder so, in denen ich nur Süßigkeiten und Eis gegessen habe. Warum auch immer). Dadurch hatte ich auch keine Schwierigkeiten nach nur wenigen Monaten wieder in meine alten Klamotten zu passen.

 

Jetzt taucht natürlich die Frage auf: Wozu eine 30 Tage Challenge, wenn die Ernährung doch paleokonform ist? Mein Ziel war es nicht Gewicht zu verlieren oder zwingend an meiner Figur zu feilen. Meine Herausforderung bestand darin auf Trockenfrüchte und Nüsse zu verzichten. Die Naschkatze in mir ist noch sehr aktiv und bei Datteln und Cashewkerne kann ich nicht nein sagen: Packung auf = Packung weg. Von wegen eine Hand voll. Meist aß ich das am Abend, was mich vermuten lässt, dass es einerseits eine saudumme (anders kann ich es nicht sagen) Angewohnheit ist. Andererseits kann es auch ein Zeichen dafür sein, dass ich tagsüber nicht genügend oder auch nicht das richtige esse. Und bisherige Versuche von zuviel Datteln und Cashewkernen loszukommen, kompensierte ich gnadenlos mit Obst. Mein Ziel war es also v.a. Zucker/ Fruchtzucker auf ein Minimum zu beschränken und das im Idealfall dauerhaft. Um zu sehen, ob ich meinen Bedarf decke, habe ich aufgeschrieben, was ich gegessen habe. Gleich vorab: Ich hatte wirklich Mühe meinen Bedarf zu decken.

 

Neben den Regeln, die Ginger für die Challenge vorgegeben hatte, verzichtete ich also auf Kartoffeln (sie schmecken mir nicht mehr), Trockenfrüchte und Nüsse/ Samen und auch Bulletproof-Coffee. Trotz oder vielleicht auch durch die Vorgabe maximal drei Früchte pro Tag zu essen, fiel mir die Umstellung erstaunlich leicht. Ich verteilte die Früchte über den Tag und so hatte ich abends nicht zwingend das Verlangen nach Datteln oder Nüssen, sondern aß stattdessen eine Birne. Das funktionierte. Es schien einfacher zu sein als gedacht – zumindest was meinen Kopf angeht.

 

In den ersten beiden Wochen habe ich mich gemäß den Vorgaben ernährt. Der Blick in mein Ernährungstagebuch zeigte jedoch meistens, dass ich unter dem Bedarf liege. Das habe ich natürlich auch gespürt: Mir wurde schnell kalt und ich hatte nach den ersten Tagen (anfangs ging es noch) permanent Hunger. Von der Laune mal ganz zu schweigen. Meinen Tag füllte ich mit vielen Zwischenmahlzeiten, die aus Eiern und Trockenfleisch bestand.
Auch die Regenerationszeit nach einem Workout (je nach Intensität des Trainings) schien sich verändert zu haben. So konnte ich nach „Karen“ – auch wenn ich während dem Workout richtig gut war – 3 Tage lang nicht schmerzfrei laufen. Der Muskelkater war richtig bitter. Mit einem kleinen Kind zu Hause ist das dann kein Spaß. Weiterhin habe ich zwei Tage nach dem Workout immer noch wahnsinnig Hunger gehabt. Wirklich Hunger. Offensichtlich hat das Workout sämtliche Reserven geleert, die ich nicht wieder so recht füllen konnte. Satt war ich dann endlich wieder, als ich zwei Tage später Thunfisch mit Ei und einen Berg Gemüse verputzt hatte – zum Frühstück. Durch Zufall bin ich auf einen Artikel gestoßen, in dem beschrieben wurde, dass Chashewkerne ein wesentlicher Magnesiumlieferant sind….Da kam dann der Aha-Effekt. Nachdem ich weder vor noch in der Challenge zusätzlich Magnesium genommen habe, waren wohl die Chashewkerne mein Hauptlieferant. So weit, so gut.

 

Ab Mitte der Challenge wurde eine Vorgabe nochmals deutlich in den Mittelpunkt gerückt: „Earn your carbs“, also Reduktion der kohlenhydratreicheren/ stärkehaltigen Gemüsearten. Das habe ich (von Beginn der Challenge an) so gut wie möglich versucht umzusetzen und habe z.B. beim Frühstück eher zur Zucchini gegriffen als zur Pastinake. Auf „Nachbauten“ habe ich verzichtet. Gleichzeitig habe ich nach rund zwei Wochen das Obst reduziert. Zunächst auf 1-2 Äpfel oder Birnen pro Tag und rund acht Tage vor Challenge-Ende dann komplett weggelassen, d.h. kein Obst, keine Nüsse, keine Riegel, keine Trockenfrüchte. Zudem habe ich die Obstmahlzeiten vom regulären Essen „entkoppelt“. Denn zuvor hatte ich immer den Eindruck, ich bräuchte noch etwas Süßes, um eine Mahlzeit abzurunden. Daher war z.B. immer eine Birne meine Nachspeise. Inzwischen bin ich wirklich happy, denn es funktioniert ohne Nachspeise recht gut. Ich habe das Gefühl, dass ich jetzt erst nach den knapp 30 Tagen auf dem richtigen Weg bin, um Zucker aus (Trocken-)Früchten wegzulassen. Daher werde ich das weitere 30 Tage machen. Nach Trainingseinheiten werde ich allerdings max. eine Handvoll Cashewkerne oder andere Nüsse zu mir nehmen, um meinen Magnesiumbedarf zu decken. Zusätzlich werde ich Supplements nehmen, um nicht wieder übermäßig viel Nüsse zu essen.

 

Zu Beginn der Challenge habe ich noch täglich drei Mahlzeiten geplant. Oftmals wählte ich als Mittagessen nur einen Salat. Aber durch Salat allein werde ich nicht satt. Auch nicht, wenn Fleisch oder Fisch dabei ist. Mein problem lag meist darin, dass ich scheinbar nie den richtigen Zeitpunkt für das Mittagessen gefunden habe. Inzwischen habe ich nun um die Mittagszeit nun eher einen Snack (Ei und Trockenfleisch) und esse am frühen Nachmittag eine Malzeit. Eine weitere Malzeit ist dann nochmal abends. Da komm ich dann gut mit Salat aus. Das komplette Essen für ein oder mehrere Tage zu planen, ist für mich nichts. Ich fahr besser damit, wenn ich so einkaufe, dass ich für mehrere Tage essen habe, ohne jede Malzeit auf den Tag zu planen.

 

Da es mir bei der Challenge nicht um eine Gewichtsabnahme ging, war ich auch wenig überrascht oder verärgert, dass sich mein Gewicht nicht änderte. Ich habe mich eh nie gewogen (in den letzten 12 Monaten drei oder vier mal). Auch hatten sich die anderen Daten (Umfang Hüfte etc.) nicht wirklich geändert. ABER: das Vorher-Nachherbild zeigte doch einen erheblichen Unterschied. Es tauchten nun erstmals Bauchmuskeln auf, die zuvor gut versteckt waren und die Hüfte ist schmaler. Saucool.

 

Seit ein paar Tagen ist die Challenge nun vorbei und ich kann noch nicht berichten, wie es mir mit Nüssen oder Trockenfrüchten geht, da ich noch keine gegessen habe. Ich bin gespannt, wie lange dieser „Zustand“ noch anhält. Meinen ersten Bulletproof-Coffee habe ich bereits genießen können. Ansonsten war der Einschnitt für mich nicht allzu groß. Ich werde allerdings darauf achten mehr nicht-stärkehaltige Gemüsesorten zu essen.

 

Fest steht, dass ich weiterhin paleo-konform esse, wie auch vor der Challenge. Ich brauche keine Nudeln, kein Getreide und auch keine Milchprodukte. Ab und an Sushi ist ok, finde ist. Aber selbst wenn die Lust auf Pizza da sein sollte, werde ich keine essen. Bei den letzten Versuchen war mir danach immer schlecht und geschmeckt hat sie auch nicht. Nach mehr als zwei Jahren kann ich nicht behaupten, dass mir was fehlt. Außer ein Glas Wein, das ich schon sehr lange nicht mehr genießen konnte und auf das ich mich richtig freue.

 

Vielen Dank nochmal für deine tägliche Unterstützung durch deine Mails und deine tollen Rezeptvorschläge in den vier Wochen 🙂

Liebe Grüße

Susanne

Nachdem ich die nutrition challenge in 2014 schon mitgemacht hatte, war für mich sehr schnell klar das ich 2016 wieder dabei bin. Meine Priorität ist die Gesundheit meines Körper. Die nutrition challenge
sehe ich als Detox und Auszeit von Zucker und Alkohol und mehr.

Damit der Einstieg nicht zu schlimm werden sollte begann ich schon eine Woche davor auf so ziemlich
alles zu verzichten und am 18.01. startete ich dann durch.  Voll motiviert habe ich eingekauft und gekocht. Lief alles gut weil mir die Produkte und Nahrungsmittel schon sehr vertraut sind. In der ersten Woche habe ich mich sehr wohl gefühlt, habe auch keinen Zucker oder Wein vermisst.
Schwieriger war das IMMER kochen, IMMER darüber nachdenken damit man alles zuhause hat und nicht in Versuchung gerät. In der zweiten Woche hatte ich mich schlechter gefühlt, wenig Schlaf, in den WODs war ich langsamer als langsam und nichts lief richtig gut. Ich musste mich durch jeden Tag schaffen.
Nachdem ich mich nun eigentlich die ganzen 30 Tage nicht gut gefühlt habe und nun merke das mein Körpergefühl langsam besser wird mache ich noch fünf Wochen (dring the open) strict weiter, damit ich den Erfolg spüre! Ich dachte vor der challenge, dass ich eigentlich ziemlich dicht an strict Paella dran bin, doch das stimmt nicht. Ich möchte noch länger viel dichter dran sein und bleiben.

Positiv ist, dass ich mich wacher fühle, meine Gedanken viel klarer sind, ich mich länger konzentrieren kann und innerlich mehr Ruhe verspüre.  Auch verlief meine monatliche Periode viel sanfter. Insgesamt verspüre ich eine Veränderung des Körpers und des Kopfes. Ich habe Lust auf mehr!
Liebe Ginger, ich bin Dir unendlich dankbar das Du das möglich machst und das Du das so professionell tust. Ich habe schon lange niemanden mehr mit Ernährungsempfehlungen vertraut, bei Dir ist das völlig anders und denke dass Du das alles 1000% erledigst.

SUPER – und DAnke , DANke, DANKE!

Ich fühle mich sehr geehrt,
Bianca

One of these years, we hope to convince all our members to try a 30-day Nutrition Challenge.  We’ve made several alterations to our basic guidelines this year in order for our participants to take the Challenge into a more individualized direction.  In this way, each Nutrition Challenge participant can receive eating guidelines that are the least-inflammatory to them as an individual, so that they can optimize their results by the end of 30 days.  There are a huge number of similarities to the Paleo Diet because paleo is by definition anti-inflammatory.  But there are also several key differences, which we feel are necessary and best supports our CrossFit athletes.

Here is our first in a series of testimonials from 2016 to assist in getting participants from among our members for the 2017 Nutrition Challenge, and hopefully to spur interest from other CrossFit boxes to offer their members the same service.  As we explained to our members, who wonder why all the services involved in each Challenge come with no price tag:  it is because the foundation of CrossFit’s success is nutrition.  So not only can you NOT call yourself a “CrossFitter” until you’ve lived through RCFN’s Nutrition Challenge, but we CAN’T call ourselves a proper CrossFit Box unless we offer the service.  Without further ado, from Vanessa, 2016 Nutrition Challenge participant:

My paleo journey started in November 2014. I had started CrossFit in October and I was looking for a way to optimize my performance along with my body composition (of course, that’s what got me started with CrossFit in the first place). I started to read more about this paleo thing everyone was buzzing about, and from time to time I heard fellow CrossFitters talk about how changes in their nutrition changed their entire lives. Well…I was pretty skeptical to be honest.

img_2853I was completely indoctrinated by the food industry. I believed that fat was bad and light products were the solution to everything. I actually believed that eating less and less would make me more and more happy. I knew (and still do!) the calories for every food. I lived and breathed brigitte diets, low-fat-high-carb-diets, not-eating-anything-at-all-diets, I once even ate only (of course light!) yoghurt for two weeks (round about 400 kcal a day) believing it was a good idea – until my mum forced me to give up on that one. I’m afraid I might have been on the brink of an eating disorder. I suppose now you get how desperate I was to shed a few pounds. The number on the scale was everything to me. Every gram was important.

Then I heard about this eating-philosophy, telling its followers to eat more fat. MORE FAT! I thought it was one of the most ridiculous things ever. Everyone knows that fat has tons of calories and that fat makes you fat. It’s what you can see on the television every day. You can read it in every magazine and every doctor will tell you to stop eating butter and eggs if you got problems with cholesterol. It just seemed so logical. Fat in – fat on your ass. Calories in – calories out. It seemed just so simple.

I don’t know what made me try my first 30-day-challenge after all. But it was the best decision I have ever made. It was the beginning of the rest of my life. It would be a lie if I told you that it was easy for me, that I just breezed through it. I have to admit that it was fucking hard! I had always hated those people who wouldn’t eat everything. Those picky people who always needed some extra shit. And suddenly I was one of them. My entire family made fun of me, my colleagues asked me whether I was going out to hunt myself some mammoths for lunch and others tried to convince me that eating raw vegetables and nuts for lunch was unhealthy and that bread would be so much better. I also decided to give up coffee, which transformed me into a real bitch for the first two weeks. The guy sharing the office with me made a point of drinking a coffee every hour or so – that didn’t help at all. But I pulled through, just sat there drinking some tea (and quietly cursed him, hoping his nose would fall off or something) because I wanted to prove to everyone that I could do it.

At that point I still didn’t really believe that paleo could change my health. But I was curious and that curiosity kept me going. So about 20 days into the challenge I began to notice some changes about the way my body was feeling. Since I was two years old I had suffered from a severe case of constipation. Sometimes I would get stomachaches strong enough to keep me from standing up. No matter what I ate or what I did, it wouldn’t get better. I went to several doctors but none of them found out what was wrong with me. They gave me prescriptions (and I had to take lots and lots of those to actually do anything against my condition – I always had a 3 month supply at home) and I figured I would just have to live with the pain or stuff my face with pills. During the challenge I had stopped taking the medicine and I was convinced the aches would be back. But they stayed gone. I was actually pain-free without taking anything! I would never have to worry about bringing enough pills when traveling. It was the first time in my life I realized, that prescriptions weren’t always the best solution. And today I’m convinced that the right food is the medication of the future!

When this realization hit me, I knew that I would never give up on paleo again. I told my mum about it and she (finally!) started to support my paleo craziness. On the 25th day of my challenge I injured myself and ended up in the hospital for about five days. It would have been easy to just let go and start eating what they served up (which actually looked really good to me!). But I had finally found a way to keep the pain away! A way to live without prescriptions! I couldn’t bear the thought of those 25 days having been for nothing. So I asked my mum to bring me a supply of cooked eggs, dried fruit, nuts, avocados and small tomatoes to get me through those days. I terrorized the hospitals catering-people (I’m absolutely positive that they had a party after I was gone…) and had them bring me the meal plan for the week and told them what components of those meals I couldn’t (well…wouldn’t ;)) eat. To make sure, they didn’t just tell me the food was free of milk, gluten and the like, I just told them I was allergic. That did the trick (can only recommend that one)!

After this first challenge I decided to stay paleo but reintroduced milk and dairy in general. I noticed that it didn’t hurt me and that I tolerated it really well. Since I just looove latte macchiato it was out of the question to completely abandon dairy products forever. But all the health benefits aside. I hadn’t lost a single pound. By that time the number on the scale didn’t matter that much anymore. But when Ginger brought another 30-day-challenge up, I wanted to give this fat-loss thing another go. And only a few days into this challenge I noticed that I had made some mistakes on the fat-loss-front the first time around. I used to eat lots of “paleo baked goods” to replace bread and lots of fruit like bananas as well as more than a hand full of nuts (cashews!!!) a day. I really enjoyed the support Ginger’s daily posts offered me. I started to eat a lot more veggies and reduced my meat consumption a bit (to make space for some rucola on my plate!).

reweI loved that all the other “fellow-paleo-rcfn-members” shared pictures of their breakfast, lunch and dinner. It really helped me reform my way of thinking about food in general and I became a lot more creative with my meals in the past month. I even started to cook 3-coursemenus for my friends and I really enjoyed planning those dinners and convincing my friends that paleo could be delicious! And they had to admit that they didn’t even miss bread, pasta or flavor-enhancers. One of them was surprised that paleo food could be “so filling” and couldn’t believe that there was nothing more in my ice-cream than frozen raspberries, a banana, ground vanilla and a sprinkle of cinnamon. I realized that it’s not about how many ingredients you put into a dish. I’d rather cook with very few, high quality ingredients and make those count. No more replacing bread or sweets with paleofied versions. And that realization was followed by fat loss.

Of course I still can’t stuff my face with tons of meat, avocado and fruit. But the numbers on the scale are going down slowly. Considering the positive effects this challenge’s had on the way my body feels, my sleep quality and my way of thinking about food (it is hard to believe how good and intense the simplest things can taste!) I don’t even care about that anymore. Paleo has changed my life. It’s as simple as that. And that is everything that counts. Now I know how good my body is designed to feel and I can’t believe that there are people out there not even willing to try this way of life for 30 days! I mean what are 30 days compared to the rest of your life, right? I wish I had found this way of life a lot earlier. I am so grateful to you Ginger and to the whole RCFN-family for their support and I have to admit I really miss those daily posts!

So, what are you waiting for?

I researched vitamin K2 (menaquinone) for my nutrition class last semester, and am excited about sharing what I found with everyone.  My intent is just to provide a small overview of everything (none of the ideas are my own – everything is quoted or paraphrased): you can get deeper into research by following links at the bottom.  Vitamin K2 has busted out only very recently into research journals, historically overshadowed by its K1 brother which not only is more plentiful in our diets, but whose role in blood clotting factors was a function understood since 1943.^21  Tiny amounts of K2 have been shown to make a significant difference not only in freedom from disease, but in vibrancy and a perfect smile.  Sound too good to be true?  Researchers have referred to vitamin K2 as “the missing nutrient” and “activator x”, but this vitamin is also rightfully referenced as the “sexy factor”:  it is linked in research I cite below with class 1 occlusion (upper and lower teeth meet where they should), freedom from tooth decay, gorgeous facial structure, strong bones, a sharp mind, fertility, and radiant health.  

Researchers believe that it was Vitamin K2 (and specifically the MK-4 isoform of vitamin K2) that Dr. Weston Price was describing in 1939 when he spoke of “a new vitamin-like activator” that worked synergistically with vitamins A and D, which were two other fat-soluble activators that he extensively studied.^1,2,3  In his book, Nutrition and Physical Degeneration, published in 1939, he devoted an entire chapter to K2 (calling it “A New Vitamin-Like Activator”), describing it as a  “unrecognized fat-soluble substance that played a fundamental role in the utilization of minerals and whose absence from modern nutrition was responsible for the proliferation of dental caries and other degenerative diseases.” ^1,2  Dr Price was a dentist who traveled around the world and studied many different cultures, conclusively finding that dental deformity and tooth decay linearly increased with degree of modernization.

There is extensive literature demonstrating “hunter-gatherers past and present have excellent occlusion, subsistence agriculturalists generally have good occlusion, and the adoption of modern foodways directly causes the crooked teeth, narrow arches and/or crowded third molars (wisdom teeth) that affect the majority of people in industrialized nations.”^2  Two researchers I respect most “believe this process also affects the development of the rest of the skull, including the face and sinuses”^1,2.  Hence, the “sexy factor”.

arches5

(the left one is sexy)

Dr. Price took samples of saliva, food, and soil with thousands of pictures, and showed that groups “isolated” from modern influence not only were eating different foods, but the foods they did have in common – vegetables and tubers, for example – contained vastly more nutrients, and were grown in soil which held a nutrient value that was “deliberately maintained”^4

The mystery nutrient was K2

Dr. Price tested samples of dairy products from around the world (by 1945 he had analyzed over 20,000 samples of butter), and found K2 to be present in fish eggs and pasture-raised animals:  their fat, organs, and their butterfat products; but only when the animals were “eating rapidly growing green grass…in most regions…the spring and early fall“.^1,4 Although Dr. Price was able to quantify the amount of K2 in thousands of samples of dairy products he received from around the world, he couldn’t describe its chemical structure, and died before the West heard about research on the vitamin by Russian scientists^1.

There were researchers who took up where Dr. Price left off, and one was Dr. Robert S. Corruccini who serves currently as a professor of anthropology at Southern Illinois University^2  He studied just under 20 cultures:  people living industrialized lifestyles all the way to hunter-gatherer lifestyles (he even included samples of some older generations with different lifestyles but the same genes) ^2.  His conclusions echoed those of Dr.Price: maloccclusion (crowded teeth & imperfect bite) is a result of changes in diet and/or lifestyle, is not genetic, and “repeatedly occurs within one or two generations‘ time” of adopting modern diet/lifestyle^2.  There is not a single exception, not a single outlier.  He also demonstrated that wild animals, including nonhuman primates, almost always show perfect occlusion^2.  Take home message?  Even if it’s too late for you, you can still save your children from a gnarly smile and thousands of euro in dental work with tiny amounts of K2.  But let’s talk about why it’s not too late even for you.  Let’s talk:

Bone density and freedom from disease

Research suggests that vitamin K2 is required in order to keep calcium out of places like arteries or other soft tissues where it could pose a risk, and calcium in places like bones where it is critically needed.  Vitamins A, D, and K2 are synergistic and essential for proper growth and health^3  Christopher Masterjohn, PhD, who created this image below, poses that bone mineralization, arterial calcification, and renal calcification should be seen as functions of the interaction between vitamins A, D and K.^12  K2 plays a critical role in the ability of bones and teeth to lay down mineralized tissue, and to the prevention of degenerative diseases of the nervous and cardiovascular systems^12,15.

v8n1-masterjohn-interactions1

1. Vitamins A and D direct cells to make proteins including the two shown on the chart above (under “bones and teeth”): Matrix Gla Protein and Osteocalcin; but K2 is required to activate them once they are made^11. Proteins Gas6 and protein S, which are involved intimately in brain function and the nervous system, also need biological activation by K2.^15

  • Osteocalcin protein organizes calcium and phosphorus absorption in the bones and teeth, and K2 supplementation has demonstrated a highly protective effect against bone fractures.^10  Vitamin K2 has a powerful influence on bone-building, and in a completely separate process facilitates a decrease in the bone-loss process^9 Vitamin K2 has been cited as one of the most frequently prescribed treatments for osteoporosis in Japan^9 Notably, in Japan where K2 is given therapeutically for people with bone problems, they describe using enormous doses of K2, up to 45 milligrams per day with no adverse effects observed^9. Can’t resist another nod to Dr. Weston Price.  Dr. Price ran a series of experiments with chickens that demonstrated that vitamin A and K2 had synergistic effects on mineral absorption of at least calcium and phosphorus^3.  He showed young turkeys fed with k2 containing butter along with cod liver oil (A and D) grew at a much faster rate than the unlucky turkeys eating only cod liver oil^3.  
  • Matrix Gla protein (MGP) is a vitamin K-dependent protein that guards against arterial calcification.  Mice lacking MGP “develop heavily calcified aortas and die prematurely”.^7  The link between K2 and cardiovascular disease prevention is a very strong one.  The Rotterdam Study was a population-based study of 4,600 Dutch men 55 years of age and older, which looked at the association of phylloquinone (K1) and menaquinone (K2) dietary intake “with the incidence of coronary heart disease (CHD), all-cause mortality, and aortic calcification”^6. This study reports food sources of MK-4 as meat and eggs, and sources of MK-5 through MK-10 as fish and fermented produce such as sauerkraut, cheese, and curds^6.  Men eating the highest K2 had 51% lower risk of heart attack mortality, 52% lower risk of severe aortic calcification, 41% lower risk of CHD, and 26% lower risk of death from all causes compared to men eating the least K2^6.  Lower risk of death from all causes means high intake of K2 doesn’t increase the risk for cancer or other major disease: you are less likely to die even from old age!^6  And “there was no consistent association of phylloquinone intake with CHD, mortality, or aortic calcification”^6. Phylloquinone is K1, found in plants:  and does nothing to minimize risk factors in this study.  Even though the 4,600 Dutch men consumed 10 times more K1 than K2, there was no relationship between K1 and any of those risk factors.^6.  The functions of many Gla proteins remain uncertain, but “are suspected to play roles in processes as diverse as bone and cardiovascular mineralization, vascular hemostasis, energy metabolism, immune response, brain metabolism, and in cellular growth, survival, and signaling”^20
  • Gas 6 is functionally “involved in a wide range of cellular processes that include cell growth, survival and apoptosis^15.  Vitamin K2 also participates in synthesizing sphingolipids, which are in particularly high concentrations in brain cell membranes^15.  Brain sphingolipids are responsive to vitamin k2 status, and “are now known to partake in important cellular events such as proliferation, differentiation, senescence and cell-cell interactions”^15.  Notably, alterations in sphingolipid metabolism are now linked to neurodegenerative diseases like Alzheimers and Parkinsons^15  Convincing data exists showing vitamin k2 influences cognition and psychomotor behavior^15  Look how clear on this chart nervous system damage is linked to fat-soluble vitamin deficiency!  Diseases which disrupt absorption of vitamins have been linked to nervous system issues, and nervous system issues resolve when absorption rates improve, just as we noted in our son ^27

 

2. K2 protects against vitamin D toxicity.  Some researchers believe that “vitamin D exerts toxicity by inducing a deficiency of vitamin K.”^12  According to this model:

“vitamin D increases the expression of proteins whose activation depends on vitamin K-mediated carboxylation; as the demand for carboxylation increases, the pool of vitamin K is depleted. Since vitamin K is essential to the nervous system and plays important roles in protecting against bone loss and calcification of the peripheral soft tissues, its deficiency results in the symptoms associated with hypervitaminosis D.  This hypothesis is circumstantially supported by the observation that animals deficient in vitamin K or vitamin K-dependent proteins exhibit remarkable similarities to animals fed toxic doses of vitamin D, and the observation that vitamin D and the vitamin K-inhibitor Warfarin have similar toxicity profiles and exert toxicity synergistically when combined.  The hypothesis further proposes that vitamin A protects against the toxicity of vitamin D by decreasing the expression of vitamin K-dependent proteins and thereby exerting a vitamin K-sparing effect.”^12

So we talked nutrition function and synergy – let’s talk structure and biochemical individuality.  

k28

Vitamin K comprises a family of fat-soluble, structurally similar, fat-soluble, 2-methyl-l,4-naphthoquinone rings (“A”).^8 Vitamin K1 (“B”: phylloquinone) differs structurally from vitamin K2 (“C” & “D”) by its monosaturated phytyl side chain located at the 3-position and the fact it is produced primarily in plants, with the highest concentrations found in green leafy vegetables^8,9.  K2 contains a polyunsaturated rather than monounsaturated side chain, and it is the number of these side chains that is indicated in its name and which influences the vitamin’s transport to target tissues.^8  K2 is synthesized by animals, and can also occur naturally, but is produced by an array of bacteria, not by higher plants^9. All forms of K2 other than MK-4 can only be produced by bacteria^8.  Bacteria do not synthesize MK-4. Instead MK-4 is produced in humans and animals by tissue-specific conversion of K1 and/or menadione ^8  Vitamin K is unique among fat-soluble vitamins in regard to its rapid loss in tissue stores, but at least in the case of K1 is ubiquitous in our diet and therefore easy to replenish^20. 

My nutrition course tasked us to name specific phases of life when people could particularly benefit from supplementation or increased natural intake of our chosen vitamin, and in the case of K2, I don’t know how you could avoid concluding that everyone could benefit in all stages of life from eating natural sources of food with high k2 intake (when defining “high” as at least 32 micrograms).  Again, not talking about supplementation of K2 – talking about targeting natural sources of K2.  Here are phases I believe I’ve shown evidence to support so far:

  • children wishing to grow normally, have good tooth structure, and maintain health
  • anyone pregnant wanting their child to have more “sexy factor”.  Also, “fetal exposure to warfarin derivatives during the first trimester of pregnancy has long been shown to result in anomalies of the central nervous system…referred to as warfarin embryopathy or fetal warfarin syndrome, includes dilation of the cerebral ventricles, microencephaly, mental retardation, optic atrophy, and blindness”^15  K2 depletion = bad when pregnant.
  • nursing mothers wishing to protect their own bones from mineral loss, and wishing to give their infant “sexy factor”
  • anyone experiencing or wishing to prevent age-related cognitive decline:
  • anyone experiencing or wishing to prevent age-related bone loss

Lifestyle factors that may uniquely benefit from K2 supplementation (and of course you would need to consult with your doctor/nutritionist) are:

  • autoimmunity:  All fat-soluble vitamins have potent immunomodulatory properties (meaning they regulate the immune system) so every one can be considered to be therapeutic in autoimmune disease.  In fact, quite a few of autoimmune diseases have been linked to fat-soluble vitamin deficiency^16,17. Quite relevant to autoimmune disease, vitamin k2 has antioxidant and anti-inflammatory properties: “emerging data…point to unique actions of…MK-4 against oxidative stress and inflammation”^15
  • osteopenia: studies have shown increased bone mineralization with high intake of vitamin K2
  • osteoporosis: Japan seems to be ahead of the bell curve on this one: recommending K2 supplementation has been part of their official guideline in treatment of osteoporosis since 1995.^25  And lots of research in support, including meta-analysis of 7 RCTs in 2006 which demonstrated significant decreases in hip, vertebral, & all other fractures following K2 supplementation.^24  K2 supplementation has been shown to not only decrease bone fractures but increase total bone strength and negate loss in vertebral height in the elderly’s lower thoracic region.^23  In one study osteoporotic women showed maintenance of bone mineral density even after 2 years with k2 supplementation^9.   Vitamin K2 exerts a more powerful influence on bone than vitamin K1, and should be considered for prevention or treatment in those conditions known to contribute to osteoporosis.^9  
  • Fish eaters:  Yes.  Vitamin K2 protects neurons from the oxidative damage induced by methylmercury^14.  Methylmercury is the predominant form of mercury in fish, and accumulates over time which is why fish at the lower end of the food chain are “safe” and the higher end carry mercury warnings.  (Because methylmercury irreversibly binds to selenium, as long as fish have higher levels of selenium than methylmercury, they don’t pose a toxin danger)
  • Alzheimer’s disease. It has been hypothesized based on existing information that chronically low vitamin K1 & k2 are risk factors for Alzheimer’s, but the hypothesis needs direct testing to verify^15.  Low k1 levels are linked to the ApoE genotype which has long been identified as a risk factor for Alzheimers.^15
  • Prostate cancer.  Dr. Mercola reported that “Increased intake of vitamin K2 may reduce the risk of prostate cancer by 35 percent, according to the results of European Prospective Investigation into Cancer and Nutrition (EPIC).  The potential benefits of K2 were most pronounced for advanced prostate cancer. Vitamin K1 intake did not offer any prostate benefits.  The findings were based on data from more than 11,000 men taking part in the EPIC Heidelberg cohort.”  Here’s the abstract but my Library doesn’t pull the full text: http://www.ncbi.nlm.nih.gov/pubmed/18400723
  • Could k2 also demonstrate a protective effect with breast cancer?  This article^19 suggests that might be true, although k2 is so new on the scene it doesn’t look as if anyone has formally tested it yet.

Drugs that cause vitamin k deficiency, requiring supplementation:

  • warfarin.  “Warfarin, a potent vitamin K inhibitor, has demonstrated adverse effects on bone remodeling and atherosclerosis”.^26  Rats fed warfarin, a drug that inhibits K2 recycling, develop arterial calcification. Feeding the rats K2 completely inhibits this effect.^14
  • Phenytoin. An anti-epileptic drug shown to induce bone loss.  K2 supplementation prevented decreased bone mass density^9
  • prednisolone. Corticosteroids are known to reduce bone formation and osteoblastic activity^9. Vitamin K2 was able to inhibit reduction of bone calcium content despite patients taking prednisolone^9.

An appropriate level of supplementation must follow a nifty chart showing the best sources of k2:  these numbers are expressed in micrograms. Might “wow” you now to understand that 1,000 micrograms is 1 milligram, and remember I wrote that the Japanese are using 45 milligrams per day doses to help people with bone problems with no adverse effects noted(!!!)

k2 sources1

You see that one pastured egg yolk (Netherlands) provides about 32 micrograms of K2.  Non-pastured eggs provide only roughly half that amount.  Research demonstrates that health preserving benefits come from remarkably small amounts of k2:  like the amount in one pastured egg yolk in the case of the Rotterdam Study.  Because Vitamin K2 is fat-soluble, you’ll notice it is found mostly in high-fat animal products including high-fat dairy, liver, & other organs.  If you happen to have daily access to one or more of these great dietary sources, there is no need to supplement with K2 unless you are dealing with some of the disease states that I’ve discussed: celiac, crohn’s or anything affecting absorption of vitamins, osteoporosis or any condition involving poor bone density, heart disease, & dental issues.  If you are supplementing, there is a synergy you need to be wary of with fat-soluble vitamins: if you supplement high dose with one fat-soluble vitamin, you must insure a proper ratio of all the others. (I got this information from Chris Kresser, but can’t find the source to give proper credit).  I give our kids cod liver oil (A & D) with their pastured eggs and they chase it with carrot juice 🙂  Consult your nutritionist for proper recommendations.

Countries which have more pastured animals offer superior sources of K2.  There are quality online sources of pastured meat such as https://www.kaufnekuh.de/.  But you also don’t need to hunt long to find it in the Nuernberg area.  Rewe supermarket now offers many different cuts of pastured meat (chicken, pork, and beef) for a reasonable price:

rewe

Kerrygold Butter (or any butter from pastured cattle) from Ireland has superior taste, and now you know it’s also better for your family’s health.  Biohof Schwarz (sold at Ebl), as well as Milchbauernhof Kleinlein in Oberasbach offer pastured eggs (but unfortunately not pastured milk).  Your purchase of these products supports not only more humane living standards for the animal you’re eating, but your own improved health and that of your kids.

1. http://www.westonaprice.org/health-topics/abcs-of-nutrition/on-the-trail-of-the-elusive-x-factor-a-sixty-two-year-old-mystery-finally-solved/ (Feb 2008)

2. http://wholehealthsource.blogspot.de/2009/09/malocclusion-disease-of-civilization.html  discusses An epidemiologic transition in dental occlusion in world populations  (http://www.ncbi.nlm.nih.gov/pubmed/6594064which Wahlstrom library doesn’t provide in fulltext. 

3. http://wholehealthsource.blogspot.de/2008/06/vitamin-k2-menatetrenone-mk-4.html

4. http://www.westonaprice.org/our-blogs/cmasterjohn/the-scientific-approach-of-weston-price-part-3-the-scope-of-prices-work/

5. http://wholehealthsource.blogspot.de/2009/10/malocclusion-disease-of-civilization_10.html

6. Dietary Intake of Menaquinone is Associated with a Reduced Risk of Coronary Heart Disease: The Rotterdam Study (2004) http://jn.nutrition.org.libproxy.bridgeport.edu/content/134/11/3100.full.pdf+html

7. Assay for Human Matrix Gla Protein in Serum: Potential Applications in the Cardiovascular Field  http://atvb.ahajournals.org/content/20/5/1257.full

8.   Menaquinones, Bacteria, and the Food Supply: The Relevance of Dairy and Fermented Food Products to Vitamin K Requirements  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3941825/

9. Vitamin K2 in bone metabolism and osteoporosis  http://eds.a.ebscohost.com.libproxy.bridgeport.edu/ehost/pdfviewer/pdfviewer?sid=d1c414c8-2823-4e56-a40c-05c508fea361%40sessionmgr4002&vid=1&hid=4110

10. Vitamin K and the prevention of fractures: systematic review and meta-analysis of randomized controlled trials.  http://www.ncbi.nlm.nih.gov/pubmed/16801507

 11.  Vitamin K2 Enhances Osteocalcin Accumulation in the Extracellular Matrix of Human Osteoblasts In Vitro  http://onlinelibrary.wiley.com.libproxy.bridgeport.edu/doi/10.1359/jbmr.1997.12.3.431/abstract

12. Vitamin D toxicity redefined: vitamin K and the molecular mechanism   http://www.sciencedirect.com.libproxy.bridgeport.edu/science/article/pii/S0306987706007171

13.  Tissue-specific utilization of menaquinone-4 results in the prevention of arterial calcification in warfarin-treated rats.  http://www.ncbi.nlm.nih.gov/pubmed/14654717

14. Vitamin K has the potential to protect neurons from methylmercury-induced cell death In Vitro  http://onlinelibrary.wiley.com.libproxy.bridgeport.edu/doi/10.1002/jnr.22630/epdf

15. Vitamin K, an emerging nutrient in brain function  http://eds.b.ebscohost.com.libproxy.bridgeport.edu/ehost/pdfviewer/pdfviewer?sid=1844d692-3f0e-4827-8f68-1c74123f1477%40sessionmgr107&vid=1&hid=108

16. Fat-soluble vitamins as disease modulators in multiple sclerosis  http://onlinelibrary.wiley.com.libproxy.bridgeport.edu/doi/10.1111/ane.12045/full

17. Overview of general physiologic features and functions of vitamin D  http://ajcn.nutrition.org/content/80/6/1689S.full

18. http://articles.mercola.com/sites/articles/archive/2008/05/03/the-vitamin-you-need-to-prevent-prostate-cancer.aspx?source=nl

19. The anticancer effects of vitamin K  http://www.cancer.cytoluminator.com/cancer-photodynamic-therapy/vitamin%20k.pdf

20. Recent trends in the metabolism and cell biology of  vitamin K with special reference to vitamin K cycling and MK-4 biosynthesis http://www.jlr.org/content/55/3/345

21. Vitamin K Metabolism http://link.springer.com/chapter/10.1007/978-1-4899-1789-8_19

22. Menatetrenone and vitamin D2 with calcium supplements prevent nonvertebral fracture in elderly women with Alzheimer’s disease  http://www.sciencedirect.com.libproxy.bridgeport.edu/science/article/pii/S8756328204003849

23. Three-year low-dose menaquinone-7 supplementation helps decrease bone loss in healthy postmenopausal women http://www.ncbi.nlm.nih.gov/pubmed/23525894

24. Vitamin K and the prevention of fractures: systematic review and meta-analysis of randomized controlled trials http://www.ncbi.nlm.nih.gov/pubmed/16801507

25. Vitamin K2 http://www.ncbi.nlm.nih.gov/pubmed/18830045

26. Vitamin K: Fracture Prevention and Beyond  http://www.sciencedirect.com.libproxy.bridgeport.edu/science/article/pii/S1934148211002425

27. Tourette Syndrome and Non-Coeliac Gluten Sensitivity. Clinical Remission with
a Gluten-Free Diet: A Description Case http://www.omicsgroup.org/journals/tourette-syndrome-and-noncoeliac-gluten-sensitivity-clinical-remission-with-a-glutenfree-diet-a-description-case-2167-0277.1000183.pdf


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