New und Updates Archives - RCF NuernbergRCF Nuernberg

Blog Archive

New und Updates

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:  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:  Certainly, knowing if you are ApoE4 homozygous or heterozygous is useful information in any prevention program.


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.


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:  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


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.


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


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. 


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.

3. European Commission’s Scientific Committee on Consumer Safety (SCCS) Opinion On the safety of aluminium in cosmetic products (27 Mar 2014).

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.

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.

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.

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.

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.

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.

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.

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.

12. Nehls, M. (2016). Unified theory of Alzheimer’s disease (UTAD): implications for prevention and curative therapy. Journal of Molecular Psychiatry, 4, 3.

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.

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.

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.

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.

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.

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.

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.

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.

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.
22.  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.
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.
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. 
25.  Raichlen, D. A., & Alexander, G. E. (2014). Exercise, APOE genotype, and the evolution of the human lifespan. Trends in neurosciences37(5), 247-255. 
26.  Puglielli, L., Tanzi, R. E., & Kovacs, D. M. (2003). Alzheimer’s disease: the cholesterol connection. Nature neuroscience6(4), 345-351.
27.  Lawrence, T. (2009). The nuclear factor NF-κB pathway in inflammation. Cold Spring Harbor perspectives in biology1(6), a001651.
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.
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.   
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. 
31. Bredesen, Dale E. “Reversing Alzheimer’s Disease” (17 Nov 2016) Silicon Valley Health Institute presentation.
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.

33. Brewer, G. J. (2016). Alzheimer’s disease causation by copper toxicity and treatment with zinc. Frontiers in aging neuroscience, 6.

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.

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.

36. Bhattacharjee, S., & Lukiw, W. J. (2013). Alzheimer’s disease and the microbiome.     

37. Bredesen, D. E. (2016). Inhalational Alzheimer’s disease: an unrecognized—and treatable—epidemic. Aging, 8(2), 304-313.

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.

39. Bredesen, Dale E (2016) Prionic Loops, Anti-Prions, and Dependence Receptors in Neurodegeneration Buck Institute for Research on Aging, Novato, California.

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.

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.

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.
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. 

44.  Hoogenraad, T. U. (2011). Paradigm shift in treatment of Alzheimer’s disease: zinc therapy now a conscientious choice for care of individual patients. International Journal of Alzheimer’s Disease, 2011. 

45. Bredesen, D. E. (2015). Metabolic profiling distinguishes three subtypes of Alzheimer’s disease. Aging (Albany NY), 7(8), 595-600.

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

47. National Institute on Aging. National Institutes of Health. “Alzheimer’s” (2015)

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”.


(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.


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.  


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:
  • 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  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:


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. (Feb 2008)

2.  discusses An epidemiologic transition in dental occlusion in world populations  ( Wahlstrom library doesn’t provide in fulltext. 




6. Dietary Intake of Menaquinone is Associated with a Reduced Risk of Coronary Heart Disease: The Rotterdam Study (2004)

7. Assay for Human Matrix Gla Protein in Serum: Potential Applications in the Cardiovascular Field

8.   Menaquinones, Bacteria, and the Food Supply: The Relevance of Dairy and Fermented Food Products to Vitamin K Requirements

9. Vitamin K2 in bone metabolism and osteoporosis

10. Vitamin K and the prevention of fractures: systematic review and meta-analysis of randomized controlled trials.

 11.  Vitamin K2 Enhances Osteocalcin Accumulation in the Extracellular Matrix of Human Osteoblasts In Vitro

12. Vitamin D toxicity redefined: vitamin K and the molecular mechanism

13.  Tissue-specific utilization of menaquinone-4 results in the prevention of arterial calcification in warfarin-treated rats.

14. Vitamin K has the potential to protect neurons from methylmercury-induced cell death In Vitro

15. Vitamin K, an emerging nutrient in brain function

16. Fat-soluble vitamins as disease modulators in multiple sclerosis

17. Overview of general physiologic features and functions of vitamin D


19. The anticancer effects of vitamin K

20. Recent trends in the metabolism and cell biology of  vitamin K with special reference to vitamin K cycling and MK-4 biosynthesis

21. Vitamin K Metabolism

22. Menatetrenone and vitamin D2 with calcium supplements prevent nonvertebral fracture in elderly women with Alzheimer’s disease

23. Three-year low-dose menaquinone-7 supplementation helps decrease bone loss in healthy postmenopausal women

24. Vitamin K and the prevention of fractures: systematic review and meta-analysis of randomized controlled trials

25. Vitamin K2

26. Vitamin K: Fracture Prevention and Beyond

27. Tourette Syndrome and Non-Coeliac Gluten Sensitivity. Clinical Remission with
a Gluten-Free Diet: A Description Case

RCFN Products online available under:

RCFN Online Shop

Our product range development is constantly growing… stay tuned

We will try having classes at 0530, 0630, 0730 and 00830 this Friday.  You MUST reschedule any class you were signed up for this Friday only!

From Friday 1000 to Monday morning the Showers will be closed for cleaning and repairs.  Sorry for the inconvenience!


The latest research performed by Brigham and Women’s Hospital (BWH) supports earlier findings that use of a light-emitting electronic device adversely impacts your health.  Participants reading on iPads [but also “eReaders, laptops, cell phones, LED monitors, and other electronic devices, all emitting blue light] took longer to fall asleep than participants reading printed books, were less sleepy in the evening, and spent less time in REM sleep.  The [electronic device] readers had reduced secretion of melatonin, a hormone which normally rises in the evening and plays a role in inducing sleepiness.  Additionally, [electronic device] readers had a delayed circadian rhythm, indicated by melatonin levels, of more than an hour.  Participants who read from the [electronic device] were less sleepy before bedtime, but sleepier and less alert the following morning, even after eight hours of sleep.

“In the past 50 years, there has been a decline in average sleep duration and quality,” stated Charles Czeisler, PhD, MD, FRCP, chief, BWH Division of Sleep and Circadian Disorders.   “Since more people are choosing electronic devices for reading, communication and entertainment, particularly children and adolescents who already experience significant sleep loss, epidemiological research evaluating the long-term consequences of these devices on health and safety is urgently needed.”   


It is well established that short-wavelength or “blue” light is the most melatonin-suppressive; this is the type of light typically emitted by devices such as televisions, computer screens, and cellphones.


Why do we care about our melatonin being suppressed?  Melatonin suppression caused by exposure to light-at-night and shift work has been definitively linked with

Obesity and metabolic syndrome:

Cardiovascular disease:


and Cancer (specifically colorectal, breast, and prostate):


What can we do?

“There are a few possible solutions for reducing your exposure to blue light at night”, claims Chris Kresser. 

“One that is commonly used in the ancestral health community is a program called f.lux, a program that makes the color of your computer’s display adapt to the time of day, warm at night and like sunlight during the day. This program can be installed on computers, iPads, and iPhones, and may have a significant effect on your melatonin secretion when using these devices at night. 

A better option, in my opinion, is to use amber-lensed goggles once the sun has gone down. These blue-blocking lenses are highly effective in reducing the effects of blue light exposure, and in most cases completely eliminate the short-wavelength radiation necessary for nocturnal melatonin suppression. (22, 23, 24) These goggles have been shown to improve sleep quality as well as mood, simply by blocking blue light and simulating physiologic darkness.

The main reason I recommend using these goggles is because normal room light alone is enough to suppress melatonin at night, and unless you’re shutting off all the lights in your house when the sun sets, you’re still at risk for disrupting your melatonin-driven circadian rhythms. (25) While f.lux is a useful tool for your backlit devices, it’s nearly impossible to address all sources of melatonin-suppressing light in today’s world of modern technology and late-night work and entertainment habits. Amber-colored goggles are one of the only tools available to completely eliminate all blue light exposure at night, without ‘going off the grid’ and powering down your entire house after 7 PM.” 

The two amber-colored goggles Chris recommends, which have received rave reviews from his patients, are the Uvex and Solar Shield brands.

See Chris Kresser’s site for links to supporting resources:

When it comes to injuries, there is one thing you should always do: seek medical advice. We are trainers, but not trained in recognizing how serious an injury is, whether it is minor or not. So, just as you go to experts when it comes to training, you should do so when it comes to injuries. If a physician is unable to tell you what went wrong and all he can say is that you shouldn’t exercise, you went to the wrong one.

That being said, there are couple of things you can expect from trainers and coaches, mainly in relation to injury prevention and rehabilitation. Before I go into that, let me introduce a couple of distinctions. Injuries are either a result of an accident or of simply overusing your body. (Of course, there are accidents, which happen due to overuse, but let’s not go there now.) You cannot really do anything to prevent accidents, in the sense that you cannot predict completely how and when they occur. Let’s say, you stand on the bus in a sloppy position, then it breaks suddenly and you fall and hurt your shoulders.

Injuries due to overuse are a different animal. One can distinguish between two types. One type occurs when you simply push hard and don’t allow your body to recover from previous workouts. Pain in the shoulders, knees, hips, or what you have is the result of performing basic movements. These should disappear once you introduce proper recovery methods such as rest days, good food, sufficient intake of Omega 3 to just name a few.

The other type of overuse occurs because one muscle group takes over some work from another group due to poor movement patterns and insufficient muscle recruitment. Not engaging the core properly when doing push ups/pull ups, presses is an example, how shoulder pain can surface. Tight hamstrings with zero gluteal activation, sets you up for lower back pain. Surprisingly, mostly the source of the problem is not where the pain actually surfaces or manifests itself.

In any case, if you ever wondered why we crawl/roll in seemingly weird positions during our warm up, there you have your answer. The aim is to activate the proper muscle groups and increase your mobility in the hips, ankles and shoulders, before we stress and tax them during our WODs or strength sessions. There is not one person who is not restricted in mobility in one or all of these areas. A warm up in the class can only play a minor role in setting you up for better and more efficient movement, so I encourage each of you to work on these areas on your own as well. RCFN coaches would be happy to assist you to get some additional fun stuff to improve your movement patterns.

As a starter, we will post some videos here from which you can select means to your own torture. Here is the first one for the shoulders. Super D is the guy with bands. Even Kelly Starrett went to learn from him some stuff. Enjoy!

Source: Reebok Crossfit Duna

Everybody has been asking for it so we got it scheduled for January 2014:





Where are you guys from originally, where do you work, and how did you meet?

Emily is from Southern California and Sven is from Bonn here in Germany. We met while both completing an exchange semester at EDHEC in Lille, France. It’s sort of funny, because neither of us really wanted to be there at the time, but it must have been fate!  Sven works at Adi and Emily at Puma… 

How do you cope with the mental anguish of continually being beaten by Emily in your CrossFit workouts?  Do you have passive-aggressive tendencies or are you gracious in defeat?

Woah! Hang on! Who said anything about being beaten?? I just let Emily win so she is happy. 

Are you attracted by the scar **still** on Sven’s forehead and why?

Well, I’m not sure I ever said I was attracted by it… But now that you mention it, didn’t Harry Potter have some kind of super powers? 

All of a sudden, you guys started coming separately to our CrossFit classes.  Shortly afterwards, we hear you ran off and got engaged.  Are these two events somehow related?  Does not working out together keep you together???  But seriously, do you find yourselves working harder when you aren’t flexing your muscles for each other and making “eyes” at each other across the room?

Do we really make eyes at each other?!  Haha anyway, our schedules have just been really busy lately so we have been squeezing workouts in when we can… Even though that means we’ve broken our 6:00amdaily routine!! 

Actually, Emily originally decided to try CrossFit when she realized that it would easily take up 100% of Sven’s free time and that she still wanted to see him once in a while! Then she was hooked, and we discovered a fun thing that we could do together and help make each other better at!
Once the excitement does down, we will be back in the normal swing of things, flexing our muscles at each other every morning 🙂
All joking aside (because of course both of you are amazing CrossFit athletes), do either of you have any goals whatsoever in your CrossFit progression, or are you just trying to continue to look good naked?

Sven: I want to get progressively better… And stay faster than Emily. 

Emily: Hm. That’s a hard question for me. Really, I just want to see what I can do. I keep getting stronger, and I want to try competing a bit and see how I like it! We will see. 
What is your favourite thing about the Nürnberg area?  how long are we going to be able to keep you in the Nürnberg area after you are “hitched”?

Easy one: the outdoor activity, the beer. And RCFN of course.  Not sure that’s enough to keep us here forever, but we will see! 

Besides CrossFit, what other interests do you share in common?

We both really like to get outside and enjoy the sunshine (an activity for which we live in the wrong location), cooking (and eating), traveling (and eating where ever we go)…. So basically: sports, traveling, relaxing, and eating. 

Thanks for featuring us!!

This year on 4 July, Emily and Sven got engaged, bringing a fiery finale to 42 months of hushed conversations, unannounced disappearances, and flushed response to casual inquiry. We managed to corner both of them in the following interview. Hope you enjoy getting to know them a little better as much as we did!


Where are you guys from originally, where do you work, and how did you meet?

Emily is from Southern California and Sven is from Bonn here in Germany. We met while both completing an exchange semester at EDHEC in Lille, France. It’s sort of funny, because neither of us really wanted to be there at the time, but it must have been fate! Sven works at Adi and Emily at Puma…



How do you cope with the mental anguish of continually being beaten by Emily in your CrossFit workouts? Do you have passive-aggressive tendencies or are you gracious in defeat?

Woah! Hang on! Who said anything about being beaten?? I just let Emily win so she is happy.



(Because Sven’s CrossFit experience in months can be determined by counting the scars littered over his body) Are you attracted by the scar **still** on Sven’s forehead and why?

Well, I’m not sure I ever said I was attracted by it… But now that you mention it, didn’t Harry Potter have some kind of super powers?


Whoa. It is definitely LOVE.


So, all of a sudden, you guys started coming separately to our CrossFit classes. Shortly afterwards, we hear you ran off and got engaged. Are these two events somehow related? Does not working out together keep you together??? But seriously, do you find yourselves working harder when you aren’t flexing your muscles for each other and making “eyes” at each other across the room?

Do we really make eyes at each other?! Haha anyway, our schedules have just been really busy lately so we have been squeezing workouts in when we can… Even though that means we’ve broken our 6:00am daily routine!!

Actually, Emily originally decided to try CrossFit when she realized that it would easily take up 100% of Sven’s free time and that she still wanted to see him once in a while! Then she was hooked, and we discovered a fun thing that we could do together and help make each other better at!

Once the excitement does down, we will be back in the normal swing of things, flexing our muscles at each other every morning 🙂


All joking aside (because of course both of you are amazing CrossFit athletes), do either of you have any goals whatsoever in your CrossFit progression, or are you just trying to continue to look good naked?

Sven: I want to get progressively better… And stay faster than Emily.

Emily: Hm. That’s a hard question for me. Really, I just want to see what I can do. I keep getting stronger, and I want to try competing a bit and see how I like it! We will see.


What is your favourite thing about the Nürnberg area? how long are we going to be able to keep you in the Nürnberg area after you are “hitched”?

Easy one: the outdoor activity, the beer. And RCFN of course. Not sure that’s enough to keep us here forever, but we will see!


Besides CrossFit, what other interests do you share in common?

We both really like to get outside and enjoy the sunshine (an activity for which we live in the wrong location), cooking (and eating), traveling (and eating where ever we go)…. So basically: sports, traveling, relaxing, and eating.

Thanks for featuring us!!


The Healthy Baby Code

Personal Paleo

Paleo Products