Acupuncture & Chinese Medicine ● Longevity Nutrition

evolution

 

Chokecherries

In the temperate zones of the Earth, late summer into autumn has been a time of celebration in many cultures. This is the time when all creatures breathe a sigh of relief as the hard work of growth slows. The cooler air transforms summer’s searing rays of sunshine into loving, golden warmth. Pregnant with sugar, fruits of flowering plants hang heavy from the branches and dapple the landscape in a mosaic of reds, blues and purples from anthocyanins and carotenoids. On the ground, combinations of lutein and zeaxanthin color the winter squashes of the Cucurbita family with the same oranges and yellows that are revealed as chlorophyll relinquishes its dominion over the foliage.

Colorful pigments that once acted as a beacon for pollinators in an array of colors and hormones[1] assume a new form that will serve as this year’s bridge of survival for numerous species of birds and mammals, including humans.

Over these precious few weeks, concentrated glucose and fructose flow in like the ocean tide. With them, the stomach’s master hormones of appetite flip flop. Ghrelin’s waxing and leptin’s waning[2] impose an ever-rising voracity of appetite that has driven successful survival of species over hundreds of millions of years. Inside the sweet goodness lurks even more treasures. Fresh omega-six oils from seeds and grains give a fresh boost to dwindling eicosanoids that are crucial for cell-to-cell communication. Vitamin E, selenium[3], vitamin C and phytonutrients stand like a levy to ensure the rising tide of inflammation doesn’t breach its banks.

In Traditional Chinese Medicine Theory, this time of year was considered the fifth season associated with the Earth element.  Warmth, sunshine, water and Earth have been magically transformed by a billion tiny seeds into a form that passes life’s nourishment unto us.   In the Jewish tradition, this season beckons the new year known as Rosh Hashanah.

“Blessed are you, sovereign of the Universe who brings forth bread to the Earth…who has kept us in life, has sustained us and brought us to this season.” Torah

Lurking deep within the cell, all the way down to the nuclear membrane, a sugar-laden surge of insulin nudges a sleeping Goddess from her torpor. 2.1 billion years ago[4],[5] some of the earliest fungi birthed this goddess and time kindly bequeathed her unto humans. In science she is known as SREBP or sterol regulatory elemental binding proteins. She is the one who, as if by magic, signals that transformation of sugar into a form that can be stored for later use as triglycerides[6] and fat[7].  Without her, most animals in the temperate and arctic zones are unlikely to survive even one winter.

Because of SREBP’s, every cell can make its own LDL cholesterol for membrane repair and vitamin D synthesis. However, without a way to supply basic antioxidants to the cell, LDL quickly oxidizes. This transformation from Dr. Jeckel to Mr. Hyde damages everything it touches[8] and is considered to be one of the driving forces of atherosclerosis7. In order to protect her inner world and ensure a constant supply of antioxidants, SREBP must ask for a little help from one of her cousins in the liver, SREBP-1. While most of the cells of the body settle for glucose as an energy source, the liver engages in a more refined taste for fructose. In fact, liver cells are the only ones that can use fructose and its effects are incendiary. Fructose drives rapid production of LDL cholesterol, fats and inflammation in the liver[9],[10]. This preference for fructose acts as a supply chain for the trillions of cells’ insatiable need for antioxidants during times like these. But without SREBP, these antioxidants are useless. She alone is the key master who permits passage of these antioxidants across the cell membrane. Under the dominion of SREBP, the LDL cholesterol receptor rises to the surface of the cell like a fish rising to feed. If it is lucky, LDL cholesterol will land in its mouth. Along for the ride, precious antioxidants like vitamins A, C, and E are granted access to the cell’s inner world[11].

As this season wanes, berries hang dried and scant on the branches. Insulin recedes as the sugar festival comes to a close. The Earth cools. SREBP breathes a deep sigh as her hard work comes to an end. As she falls into her winter nap, she brings many of the creatures of the Earth with her. Only one creature has successfully escaped the dominion of this goddess. Humans innovated to store carbohydrates externally. This consistent supply of sugar drives insulin to ensure that SREBP never sleeps. Her unrelenting state of slavery drives disorders like obesity[12],[13], fatty liver[14], insulin resistance[15] and atherosclerosis[16], [17]. Perhaps this goddess would argue that these are not diseases at all but are phenotypes brought on by depriving her of a proper rest.

[1] Cutler A.J., Krochko J.E. Formation and breakdown of ABA. Trends Plant. Sci. 1999;4:472–478. doi: 10.1016/S1360-1385(99)01497-1

[2] Teff KL, Elliott, SS, Tschop M, Kieffer TJ, Rader D., Heiman M., Townsend RR., Keim NL, D’Alesso D, Havel Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. PJ J Clin Endocrinol Metab. 2004 Jun;89(6):2963-72

[3] Giacomo dugo, Lara La Pera, Donatella Pollicino, marello Saitta. Determination of Selenium Content in Different Types of Seed Oils by Cathodic Stripping Potentiometry (CSP) J. Agric. Food Chem., 2003, 51 (19), pp 5598–5601

[4] Timothy F. Osborne, Peter J. Espenshade Evolutionary Conservation and Adaptation in the Mechanism that Regulates SREBP Action: What a Long Strange tRIP It’s Been. Genes & Dev. 2009. 23: 2578-2591, doi:10.1101/gad.1854309

[5] V Laudet Evolution of the Nuclear Receptor Superfamily: Early Diversification from an Ancestral Orphan Receptor. Journal of Molecular Endocrinology Dec. 1, 1997. 19 2-7-226

[6] Colleen K. Nye  Glyceroneogenesis Is the Dominant Pathway for Triglyceride Glycerol Synthesis in Vivo in the Rat The Journal of Biological Chemistry, 283, 27565-27574.  October 10, 2008

[7] Hitoshi Shimano, SREBPs: physiology and pathophysiology of the SREBP family. The FEBS Journal 2009 276:3 616-621

[8] Low Density Lipoprotein Can Cause Death of Islet β-Cells by Its Cellular Uptake and Oxidative Modification Miriam Cnop, Jean Claude Hannaert, Annick Y. Grupping, and Daniel G. Pipeleers Endocrinology 2002 143:9 , 3449-3453 http://dx.doi.org/10.1210/en.2002-220273

 

[9] Zhang C, Chen X, Zhu RM, Zhang Y, Tu T, Wang H., Zhao H, Zhao M, Ji YL, Chen YH, Meng XH, Wei W, Xu DX. “Endoplasmic reticulum stress is involved in hepatic SREBP-1c activation and lipid accumulation in fructose-fed mice.” 2012 Aug 3;212(3):229-40. doi: 10.1016/j.toxlet.2012.06.002. Epub 2012 Jun 12.

“ER stress contributes, at least in part, to hepatic SREBP-1c activation and lipid accumulation in fructose-evoked NAFLD.”

[10] Koo HY, Miyashita M, Cho BH, Nakamura MT. Replacing dietary glucose with fructose increases ChREBP activity and SREBP-1 protein in rat liver nucleus. 2009 Dec 11;390(2):285-9. doi: 10.1016/j.bbrc.2009.09.109. Epub 2009 Sep 30.

“Nuclear SREBP-1 was 2.2 times higher in fructose-fed rats than glucose-fed rats.”

[11] Maret G Traber, Herbert J Kayden “Vitamin E is Delivered to Cells via the High Affinity Receptor for Low-Density Lipoprotein” The American Journal of Clinical Nutrition 40: October 1984, pp 747-51.

[12] Hitoshi Shimano, SREBPs: physiology and pathophysiology of the SREBP family. The FEBS Journal 2009 276:3 616-621

 

[13] Hitoshi Shimano, SREBPs: physiology and pathophysiology of the SREBP family. The FEBS Journal 2009 276:3 616-621

[14] Moon YA, Liang G, Xie X, Frank-Kamenetsky M, Fitzgerald K, Koteliansky V, Brown MS, Goldstein JL, Horton JD. The Scap/SREBP pathway is essential for developing diabetic fatty liver and carbohydrate-induced hypertriglyceridemia in animals. Cell Metab. 2012 Feb 8;15(2):240-6

[15] Iichiro Shimomura, Robert E. Hammer, James A. Richardson, Shinji Ikemoto, Yuriy Bashmakov, Joseph L. Goldstein,Michael S. Brown

Insulin resistance and diabetes mellitus in transgenic mice expressing nuclear SREBP-1c in adipose tissue: model for congenital generalized lipodystrophy. Genes Dev. 1998 October 15; 12(20): 3182–3194.

[16] Karasawa T, Takahashi A, Saito R, Sekiya M, Igarashi M, Iwasaki H, Miyahara S, Koyasu S, Nakagawa Y, Ishii K, Matsuzaka T, Kobayashi K, Yahagi N, Takekoshi K, Sone H, Yatoh S, Suzuki H, Yamada N, Shimano H. Sterol regulatory element-binding protein-1 determines plasma remnant lipoproteins and accelerates atherosclerosis in low-density lipoprotein receptor-deficient mice. Arterioscler Thromb Vasc Biol. 2011 Aug;31(8):1788-95.

[17] Kurtak, K. Dietary and Nutritional Manipulation of the Nuclear Transcription Factors, PPAR’s and SREBP’s, as a Tool for Reversing the Primary Diseases of Premature Death and Aging. Rejuvenation Research 17-2. April 2014. P 140-44.

 

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A wise shaman once said, “Don’t confuse compassion with sacrifice. The divine mother is a warrior who is fierce, fearless and full of compassion.” She does not bring forth life into this world with the dainty beauty that has befallen the stereotype of women. She births life as a bloody, ripping warrior whose battle cries reverberate through her body with the echo of a billion lives that came before her. Some made it. Most never survived that journey. Under the escort of Kali, they returned into loving arms of the place from where we all came. And here you stand on this Earth. One of the few whose DNA survived the journey over billions of years. One who survived the War of Nature[1] long before mammals even existed. Who survived famines and floods, droughts and disease, fires, volcanoes, and ice ages. One who defied predation. Much later your genetic material survived tribal wars and world wars, injustices, abuses and epidemics. Your DNA even survived childbirth. Along the journey, your triumphs picked up many friends along the way.

In 1953, Watson and Crick’s discovery of DNA opened our naïve minds to the possibility that life could be as simple as a blueprint. Seemingly endless combinations of codons have been passed from generation to generation from the genesis of life itself. As we sorted through the simplicities of blue or brown eyes, red or blond hair, our genome taught us that an entire existence has come with us that we still don’t completely understand. What we once thought was “junk DNA” was later discovered to be our viral ancestors. One was given the name ERVWE1. Her very presence birthed our own ability to carry out placental development and thus, embryo survival[2].  Through coding for a protein called syncytin[3], she grants sperm and egg another chance to come together for another shuffle of adenine, cytosine, guanine and thymine. Without her, mammalian mothers cease to exist.

Later we discovered completely different type of DNA inside each cell that has nothing to do with the color of our eyes. This DNA resides inside the cell’s mitochondria and enables almost all living beings to convert food into energy. It is a bridge for nutrients between our inner world and Mother Earth. Whether it autogenously developed on its own or came from an ancient bacterium is still a mystery. Unlike the DNA that is passed on from the union of male and female, mitochondrial DNA comes exclusively from the mothers who have passed it through ova from generation to generation.

 

Another universe of genetic material that is passed from the mother is the microbiome. This is “the ecological community of commensal, symbiotic, and pathogenic microorganisms that literally share our body space.”[4],[5]. These various bacteria, fungi, parasites and viruses provide signaling that influences the inner workings of our entire body.   They support immune function, moderate inflammatory responses, generate vitamins that we are not capable of making, produce hormones from some of the foods we eat, help us to absorb minerals, and regulate the production of neurotransmitters. Most importantly, they allow our immune system to remain competitive with the rate of evolution of pathogens.

Comprised of the same creatures found in the Earth itself, this genetic material that we carry inside us has been passed down through thousands of generations. Most animals on the planet, including many (and possibly all) born through eggs[6] receive this life-giving inoculation of Earth as they pass through their mother’s birth canal.

Just a few years ago on February 15th, 2001 we saw our first glimpse of a complete human genome published in the journal Nature. What we thought was a blueprint for solving the mysteries of human disease quickly clouded our concept of the things that us grant us a long and healthy life. Numerous studies appearing in prestigious journals have shown us again and again that genetics plays only a small role in the outcome of our lives[7] [8] [9]. In fact, as little as 10% of our health and longevity is determined by our genetic programming. The rest comes from the daunting myriad of external influences encompassed by entire universes about which we know very little. After all, we’ve only cultured and identified less than 1% of the life within soil, which carries the same microorganisms as our bodies.   The rest is still a mystery. Perhaps understanding them from a scientific basis carries little merit. Wisdom has been passed down in many forms. The original innate wisdom requires no explanation. Its knowledge lies in the very fact that we share this space and time with millions of other creatures whose DNA also survived this epic journey. Because they are here, we are here. Compliments of the fierce compassion of our mothers who carried forth pieces of The Living Goddess.

[1] Darwin, Charles M.A. On the Origin of Species by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life. 24 November 1859. Nature 1st ed.) (London: John Murray) p. 503

[2] Lavialle C, Cornelis G, Dupressoir A, Esnault C, Heidmann O, Vernochet C, Heidmann T. (Aug 2013). “Paleovirology of ‘syncytins’, retroviral env genes exapted for a role in placentation.”. Philos Trans R Soc Lond B Biol Sci. 368 (1626). doi:10.1098/rstb.2012.0507. PMID 23938756

[3] Esnault C, Cornelis G, Heidmann O, Heidmann T (2013) Differential Evolutionary Fate of an Ancestral Primate Endogenous Retrovirus Envelope Gene, the EnvV Syncytin, Captured for a Function in Placentation. March 23, 1013. PLoS Genet 9(3): e1003400. doi:10.1371/journal.pgen.1003400

[4] Lederberg J, McCray AT. ’Ome Sweet ’Omics—a genealogical treasury of words. Scientist. 2001;15:8

[5] The NIH HMP Working Group. 2009. The NIH Human Microbiome Project. Genome Res. 2009 December; 19(12): 2317–2323.

[6] University of Georgia “Healthy Intestinal Bacteria Found Within Chicken Eggs.” Science Daily June 3 2008.

[7] Prof Salim Yusuf DPhil,Steven Hawken MSc,Stephanie Ôunpuu PhD,Tony Dans MD,Alvaro Avezum MD,Fernando Lanas MD,Matthew McQueen FRCP,Andrzej Budaj MD,Prem Pais MD,John Varigos BSc,Liu Lisheng MD,on behalf of the INTERHEART Study Investigators Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study

The Lancet – 11 September 2004 ( Vol. 364, Issue 9438, Pages 937-952 )

DOI: 10.1016/S0140-6736(04)17018-9

[8] Mozaffarian D, Kamineni A, Carnethon M, Djoussé L, Mukamal KJ, Siscovick D. Lifestyle Risk Factors and New-Onset Diabetes Mellitus in Older Adults: The Cardiovascular Health Study. Arch Intern Med. 2009;169(8):798-807. doi:10.1001/archinternmed.2009.21.

[9] Steingraber, Sandra. Living Downstream.   Reading, Mass., Addison–Wesley, 1997 “80% of all cancer is attributable to environmental [external] influences.”(Steingraber, 1998 p 60)

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With the best of intentions are we slowly rendering our population incapable of developing natural, adaptive immunity?  In his upcoming book, Doc, Terry Grossman M.D. gives a powerful example of this as he discusses the pros and cons of vaccines.  I would like to expand on the subject.

In 2005, a study by W Katherine Yih et al, was published demonstrating that from 1998-2003 “As varicella vaccine coverage in children increased, the incidence of varicella (chickenpox) decreased [by 79%] and the occurrence of herpes zoster (shingles) increased [by 90%]”. These figures are beyond statistically significant.  Similar trends were observed in several areas where the varicella vaccine was initially introduced.  The explanation for the unexpected emergence of shingles was this.  In any given population, there would have been an ongoing percentage of people with active varicella infection.  Chronic, low-grade exposure to the virus throughout the population ensures that it remains on the immune system’s “radar screen” and is therefore kept at bay by our own adaptive immunity.  Vaccinations work in a similar fashion.  Another study done by Bryson et. Al. predicted that “a substantial increase in herpes zoster cases over the first 30–50 years after the initiation of mass vaccination, peaking about 20 years after the start of mass vaccination at an incidence of 51 percent over the pre-vaccination level and eventually falling below the initial incidence”. doi: 10.1016/S0264-410X(02)00180-9  Another study conducted in Germany also concluded there was sufficient evidence to suggest that varicella vaccinations lead to higher incidents of herpes zoster in the older population.

To be objective, before 2003, herpes zoster was not identified as a nationally notifiable disease, and no states in the US required reporting of cases.  The study mentioned above seems to have accounted for record discrepancies within the chosen test site.  However, a study came out in 2008 doi: 10.1086/522162 demonstrating that some areas where the varicella vaccine was introduced saw minimal change in reporting of herpes zoster cases.  There is one claim in this study that I take major issue with. They state “Evidence from population-based studies suggests that rates of HZ [herpes zoster] were increasing in the United States before the introduction of the varicella vaccination program.”  Another study  states that the incidence of herpes zoster has been increasing since 1945.  In both of these studies, several crucial data points were not accounted for.  First, there was no oversight or requirement in reporting of herpes zoster events before the introduction of the vaccine in 1995.  Second, access to health care has increased between 1945 and the present.  Reports of incidents would not have been consistent through any subsection of the general population.  I’m not saying they don’t have some valid points but in a scientific paper, these are presumptive and irresponsible statements.  Their conclusion should have been that the data is inconsistent and not available.

There are always unknowns.  However, the current research suggests that the introduction of the varicella vaccine saved an average of 90 lives per year and created an anthropogenic chasm in an entire system, between virus and human, that had evolved over the millennia to reach a steady state.  Trends like this have the potential to remove human beings from the interconnected web of Evolution and Natural Selection.  In this way, technology loses its place as a luxury and instead becomes a necessity of human survival.

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Hello to all of you wonderful people who have taken time out this precious life to read my blog. I had to check out for a while due to some personal tragedy. As some ancient cultures say ” I have been waiting for my soul to catch up with the rest of me” and I am FINALLY starting to write again. Upcoming subjects include:
-Evolution Dictates a Contrarian Approach to the Emergence and Spread of Human Pathogens
-Misinterpretation of Methylation. Why Folic Acid Doesn’t Cause Cancer
-A Conventional Interpretation of the Four Levels of Disease in Traditional Chinese Medicine
-A Conventional Interpretation of Digestion in Traditional Chinese Medicine
-Why We Need to Introduce a New School of Research if Science it Going to Successfully Evolve

I look forward to more great discussions and comments.

Sincere thanks to each of you!
Karen

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Human beings constantly strive to be more than what we think we are.  We look outside of ourselves for the next thing to make us smarter or younger, stronger or live longer.  This yearning has given birth to the multi-billion dollar industry of nutritional supplements.  We are subject to a continuous stream of advertising and information on the next great discovery.  If you drink this berry juice from the Amazon you will live longer!  Take this new antioxidant discovered in these roots from some exotic part of China!

What are we really discovering?  That the fruits and roots and herbs and leaves that come from our Earth are good for us? These are not new discoveries.  The discovery is that these foods are what we should be eating!  From red wine to tobacco, amazing health-giving qualities can be found in any real food that we consume.  The ancient civilizations like China and India have known this for hundreds if not thousands of years.  Their diets have evolved to the point that their day to day meals are their medicine.   

Let’s take the seemingly miniscule example of folic acid.  Its name is derived from its source, foliage.  One study after another has shown the incredible health-giving benefits of folic acid.  To name a few:  reducing the incidence of birth defects, reducing the incidence of lung cancer in smokers and several other types of cancer, reducing the risk of Parkinson’s disease, and increasing fertility in both men and women. I can’t tell you how many women I have seen for infertility who became pregnant within a month of two of taking large doses of folic acid along with B6 and B12.  Folic acid has perhaps a couple hundred biochemical functions in the body.  One of the more interesting is its ability to turn genes off by giving up (donating) part of its chemical makeup known as a methyl group. (many other vitamins and substances do this as well). 

In the emerging field of epigenetics one of the most mind-blowing experiments done to date was with Agouti mice.  Scientists use a genetic strain of mice known as “Yellow Mice” which have a high risk of cancer, diabetes, obesity and reduced lifespan to study these very diseases.  They discovered that when they fed pregnant “Yellow Mice” folic acid, not only did the offspring look completely different (leaner, brown-gray fur, etc) but even feeding the offspring the same disease-inducing diet as the “Yellow mice”, the offspring had lower incidences of cancer, obesity, diabetes and lived longer!  This “new” strain of mouse was called the Agouti mouse even though it was genetically identical to its predecessor.  Discoveries like these in epigenetics are forcing scientists to reconsider major theories like “nature vs. nurture” and certain mechanisms in the theory of Evolution. 

On the flip side a few studies have come out recently showing that folic acid supplementation increases the incidence of some types of cancers especially in the prostate.  We have to consider that everything in nature functions as part of the whole.  When we eat green, leafy vegetables we receive not only folic acid but also an array of B vitamins and trace minerals which so often function with folic acid in the body.  We also receive hundreds of plant chemicals that alter how our genes control our immune systems, detoxification pathways, etc.  This is what we evolved with. The more we delve into the awesome intricacies of Mother Nature, we reach two realizations.  (1)How little we know.  (2) We already know everything because we evolved with it and are a part of it. 

So what it the conclusion I am asking you to come to today?  Is it that you should take more folic acid?  Perhaps it’s not that taking large doses of folic acid is good for us.  It’s that NOT consuming it in the amounts and forms that we evolved with is making robbing us and our progeny of our health and vitality.  Imagine living before farming.  What do you think you would eat in the springtime?  Look around at what is emerging from Earth.  What are you made of?

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This is a continuation from the previous post in which one of my readers asked about methionine restriction as it relates to longevity and methionine content in eggs.  I never claim to be “the knower of the answer” but I like to provide enough information for people to form their own, and perhaps new, ideas.

 As I mentioned last time an increase in metabolism will always result in an elevation of all ROS in cells.  This, by default, speeds cell turnover and aging.  Inversely, reduced metabolism reduces turnover and aging of cells.  This is the same mechanism through which caloric restriction is theorized to promote longevity.   

Restriction of any substance that is severe enough to slow down metabolism causes the mind and body to go into a torpor-like state.  If it doesn’t, damage is incurred.  I see this regularly in my practice as a condition that I have termed “Boulder Syndrome” which I’ve talked about in previous posts.    

It seems that in order to live longer though means of dietary restriction, you have stop fully living or suffer health consequences.  Take SAMe as an example.  SAMe is made from methionine in the liver and acts as the rate limiting step in the production of several neurotransmitters. These include dopamine, serotonin, norepinephrine and its conversion in the brain to epinephrine.  Low levels of these neurotransmitters tend to reduce mental clarity, motivation, drive and overall energy.  This is likely part of the whole conservation mechanism that would naturally slow down the body in times of protein scarcity.

Eggs are so interesting because they contain all the essential nutrients to carry out Phase 1 detoxification and methylation in the liver (choline, methionine, magnesium, B12, B6 and folate).  It happens that a deficiency of any one or more of these essential nutrients has a documented effect on reducing fertility. (Sorry, I just didn’t have time to find that many references for one statement but I can assure you it is a fact).   As I mentioned in the previous post, this could be from some type of signaling from Phase 1 that would indicate the presence of sufficient nutients available for reproduction.  I suspect that if the above nutrients are scarce, Phase 1 probably slows for the purpose of conserving them to maintain other bodily functions more consistent with survival and not reproduction.

Consider how we evolved eating eggs.  In non-tropical zones, eggs are in abundance mainly in the spring and early summer.  As the weather warms the insects hatch providing a sustainable protein source for birds.  The increase in dietary protein, and thus methionine, in birds’ diets would signal the appropriate anabolic processes for them to become fertile and produce eggs.  A few weeks later, early humans would have access to these eggs which would provide the appropriate nutrients for signaling anabolic processes to start preparing them for reproduction.  Methionine moves like a wave through the food chain, from sulfur in soil to plants to insects to birds to humans, signaling the anabolic processes that enable reproduction.

In tropical zones, eggs would have been available most of the time as would an abundance of nutrients that would support reproduction. This scenario applies more to the people of the developed world.

I don’t think simple reduction of dietary methionine intake is sufficient enough to slow aging.  I think it has to be fairly extreme.  Alternatively, I do think that excess amounts of methionine, which would imply excess amounts of protein could be damaging especially if intake of magnesium, folic acid, B12 and B6 is insufficient.  We also have to consider that if we reduce methionine enough to slow down metabolism, caloric consumption must be reduced as well or the slower metabolism will lead to weight gain.

That said, if you would still like to try to reduce your dietary methionine here are some things to consider.  With regards to dietary intake, you have to look at absorption rates. This is influenced by the ratio of methionine to the other amino acids in the protein source.  As a general rule, amino acids will compete with one another for absorption. For example, if you have low levels of threonine, high valine levels inhibit the absorption of methionine  (Anyone want to research which protein sources have these ratios? Good data at http://www.nutritiondata.com/ )  The higher the ratios of other amino acids the lower the absorption will be of methionine.  Animal proteins contain high levels of methionine but much higher ratios of the various other amino acids so ultimately methionine absorption is diminished. I checked some methionine levels in various protein sources and unfortunately got varying results.  It turns out that methionine content of food is related to sulfur content in the soil so there will be significant variability depending on the geography of the food source.  However as a general rule, cottage cheese, eggs and fish were all similar in methionine content. Pork and poultry were a bit higher.  Beef was high but had really high levels of competing amino acids.  Legumes and seeds were much lower.  NOW FOR THE INTERESTING PART.  It has been suggested that a vegan diet offers less methionine and would contribute to longevity through methionine restriction.  However, I found a study done on amino acid absorption in rats.  It turns out that pinto beans, one of the least rich protein sources of methionine, had the highest absorption rate the amino acid.  I’m sure absorption of methionine from soy is low as well because some of the chemicals in soy interfere with overall amino acid absorption.

However, soy introduces an extremely important consideration that might make it impossible for humans to benefit from methionine restriction.  Soy contains estrogen-mimicking phytochemicals which will have some effect on producing anabolic processes. (the exact thing we’re trying to prevent to extend longevity) These chemicals must be detoxified by Phase 1 enzymes in the liver.  If this pathway is not working because of a deficiency of methionine, folic acid etc then there will be accumulation of these chemicals in the fat tissues possibly increasing incidence of hormone-sensitive cancers.  There are hundreds of anabolic hormone-mimicking chemicals that are now ubiquitous in our environment including BPA, several pesticides and hormones from pharmaceutical use. Any steps taken to reduce methionine will slow detoxification of these chemicals to a trickle.

If you want to continue to think creatively, be active, fully participate in life and be able to detoxify various environmental chemicals,  you have no choice but to consume foods that allow your body to do this.  If you want to attempt to extend your life through the means of caloric and methionine restriction then you will spend your life existing, not fully living and you might still get cancer.  Perhaps one way of using the current knowledge of caloric and methionine restriction to extend life is to follow what would naturally happen with the seasons.  For example, reduce your activity in the winter and practice caloric and methionine restriction.  Personally, I love skiing too much and need lots of protein to be able to do it.   That said, I’m going to continue to eat 8-10 eggs per week along with lots of kale.

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One of my readers questioned my recipe from “If Popeye Was a Real Man He Would Have Eaten Kale” and asked what I thought about the research linking longevity and methionine restriction. Eggs are a significant source of methionine and so perhaps could lead to faster aging.  In order to answer this question, it’s important to consider the mechanisms involved and the evolutionary advantages.   This question enters one of the world’s biggest rabbit holes and is too much for one posting so watch for posts related to methionine restriction and longevity in the future. 

To review, several research studies have shown that dietary restriction of the essential amino acid, methionine, results in 42-44% increase in average life span of rats, mice and fruit flies.  There are two major mechanisms that have been identified that contribute to this.  One is lowered production of mitochondrial reactive oxygen species (mROS).  These are basically free radicals produced in the mitochondria where our cells make energy or ATP.   mROS speed up degeneration of mitochondrial DNA, ultimately leading to faster cell turnover and aging.  Glutathione (GSH), is one of the most powerful reducers of mROS.  GSH is made from methionine.  However, restricting methionine intake results in elevated levels of GSH in all tissues except for the kidneys.  How is it that restricting methionine, the one essential amino acid that is a precursor to glutathione, results in higher levels of glutathione? It’s going to be very interesting when researchers figure out the answer to the dichotomy. 

With regards to longevity, I think methionine restriction has two contributing factors.  I’ll discuss one of them here and leave the second for another time.  Here is the first: 

Since methionine is an essential amino acid and is present in all naturally-occurring protein sources, it likely acts as a signal for protein abundance or scarcity.  Cellular signaling mechanisms are too involved for this discussion.  To simplify I’ll just say signaling may directly due to the presence or absence of methionine or may be through a secondary metabolite like homocysteine.  If its presence signals abundance, then the body would increase metabolism as it goes into an anabolic state preparing for reproduction.  An increase in metabolism will always result in an elevation of all ROS in cells.  This, by default, speeds cell turnover and aging.  On the other hand, if protein intake, and thus methionine, is scarce then the body likely creates different signals that reduce metabolism.  Reduced metabolism reduces turnover and aging of cells.  This is the same mechanism through which caloric restriction is theorized to promote longevity. 

With methionine, this control mechanism would incur an ultimate evolutionary survival advantage.  We know that methionine restriction reduces fecundity (reproductive ability).  During times of protein scarcity reduced metabolism via this signaling mechanism would minimize ongoing damage to mitochondrial and cellular DNA.   This would help to preserve the potential for successful reproduction (passing on of genes) and to prolong existence in anticipation for a more abundant and auspicious time.  As mentioned, in times of protein abundance, methionine would signal anabolism and preparation for reproduction.   If an individual is past reproductive age, metabolism will still increase.  In a community setting the increased vitality of older individuals would allow them to contribute more in the short term.  In this situation, survival advantage would be incurred throught The Grandmother Hypothesis .  It would also speed its ultimate demise, freeing up resources for the younger individuals who can still reproduce.

Since we, in the first world, live in a state of perpetual abundance we have time to figure out how we can live longer.  Restricting dietary methionine may likely contribute to this.  It seems logical that you would simply restrict foods that contain high amounts of methionine.  However, it isn’t that straight forward.  Next time I will discuss the glutathione dichotomy and methionine’s role in the alternation between Phase 1 and Phase 2 liver detoxification, the intricacies of dietary amino acid absorption, and research that contradicts the hypothesis that a vegan diet reduces methionine intake.  Yes, the egg question will finally be answered.

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New ideas regarding human evolution are blossoming from 6 million year old fossils found in Ethiopia.  Nova’s three-part series, “Becoming Human” debuted November 3rd on Nova on PBS.  Even if you missed the first one the rest will most certainly be  illuminating, with discussions at every level of our ever-evolving  planet.  It may also give the adventurous some interesting travel ideas.  Enjoy!

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