Dr Tetyana Obukhanych, Ph.D. - Natural Immunity and Vaccination

Dr Tetyana Obukhanych, Ph.D. - Natural Immunity and Vaccination

Ukrainian-born immunologist, Dr Obukhanych PhD is the author of Vaccine Illusion: How Vaccination Compromises Our Natural Immunity and What We Can Do to Regain Our Health. In her book, she presents a view on vaccination that is radically different from mainstream theories
Dr Tetyana Obukhanych, has studied immunology in has studied immunology in some of the world's most prestigious medical institutions. She earned her PhD in Immunology at the Rockefeller University in New York and did postdoctoral training at Harvard Medical School, Boston, MA. and Stanford University in California.

She does talks for mom groups, practitioners and WAPF groups. I just saw her in SF on Sunday. She's absolutely wonderful and super brilliantly sharp!

Her view on the science is clear, concise and complete. Her intention is to illuminate the science, not perpetuate the public health fears. Facts v. fiction. The goal of the talk is to review: the facts, the theories, the choices.

"Facts without theory are nonsense. And theories without facts are b*llsh*t."

--Dr Obukhanych's favorite stat professor at Stanford

In her latest talk, she discusses some immunoprotective strategies and their mechanisms in health:

--vitamin C

--vitamin A (her favorite is WAPF supported, fermented CLO, cod liver oil)

--vitamin D

--probiotics

--raw dairy, cream, raw eggs

--breastmilk as a shield for the baby and why (AHS14 The first paleo food: Breastmilk and it's alive! Speaker: Dr Goscienski MD)

Phat Fat Mitochondrial Energetics: Mobilization v. Accumulation

Adipose is Alive

In ancestral times, adipose stores may have determined longevity and survival past harsh cold winters. My ancestors moved from northern China 8-10+ generations ago to the mountainous areas of Taiwan (according to my dad several hundred years ago). I suppose those who didn't live past the impoverished seasons where food resources were scarce would not have made it, nor would their genes. I can thank them for my persistent fat stores *haa*. Adipose tissue is an endocrine gland which is know to secrete hormones such as leptin and adiponectin to control hunger, body energy balance and energy expenditure. These hormones are involved directly with mitochondrial biogenesis as well, in other words the production and destruction of the mini powerhouses found in all cells (except perhaps glycolytic-dependent cancer cells, which I think are all of them).

Whole body energy balance are determined by many factors, including most importantly:
1) demand
2) diet
3) d*ng hormones (or lack of)



All Organs Sync For Survival

Our brain coordinates many of the hormones that either mobilize or store adipose, e.g. fat. The brain includes the hypothalamus, pituitary, pineal, forebrain, hindbrain, midbrain and our senses for perception (ears, eyes, nose, taste, temperature, barometric pressure, etc). For example, insulin is triggered cephalically (via the brain): by tasting sweetness whether artificial or real, by smelling food, seeing food or even imagining food. Hearing? Hearing the neighborhood ice cream truck as a kid?




Humans Killed for Fat

Fat may have been the biggest boon for man during evolution (see prior animal pharm: humans as marine-based carnivores). Fat contained omega-3s concentrated up the food chain from green chlorophyll sources (grass, algae, etc) and into the muscle fat, organ meats, brains and fat stores of animals and seafood. The encephalization of ancient man is believed to be highly associated with the intake of dietary omega-3s. Perhaps the current de-encephalization over the last 100 yrs is related to the relative deficiency of dietary omega-3s? Or growing overabundance of omega-6s? THANK YOU VERY MUCH corn-fed cows and Keys.




Fat Yields the Most Energy in Human/Mammalian Energy Systems

Hormones for MOBILIZING fat stores far out number the hormones that ACCUMULATE fat. See diagram, modified from Gary Taubes GCBC from a 1965 table of hormonal regulation. Forgive me I use the term 'hormone' loosely because food is hormonal. Fatty acids bind PPAR receptors. We have ~ 3-4 routes to produce energy (some cells utilize glutamine, but I don't know which... neurons only?). Burning fatty acids yields the highest net energy unit (ATP). Why I've wondered? So many hormones promote the escape of fatty acids from temporary storage -- intramuscular, liver, visceral fat, brown fat and subcutaneous fat. Why do we readily release fatty acid energy? Sex, power, survival/suicide? Heat for 37C?

Taubes quoted Hans Krebs who received the Nobel in Medicine in 1953 'All three major constituents of food supply carbon atoms.. for combustion." GNG= gluconeogenesis (glucose/glycogen from any source -- protein, fat, carbs); ATP lesson (click HERE and UCD Lecture and med biochem):



Low Yield but Mandatory Without Oxygen
--anaerobic glycolytic (glucose/GNG) [Yield: 2 ATP]


High Yield in the Presence of Oxygen
--aerobic glycolytic (glucose/GNG) [Yield: 38 ATP] 
--aerobic beta-oxidation of fatty acids like palmitate [Yield: 129 ATP]
--aerobic beta-oxidation of fatty acids like stearate [Yield: 146 ATP]
--aerobic beta-oxidation of fatty acids like ketones [Yield: 51 ATP]
--aerobic oxidation of alcohol [Yield: 16 ATP]


Carbon lengths:
Glucose: 6-carbon carb
Palmitate: 16-carbon saturated fatty acid
Stearate: 18-carbon saturated fatty acid
Ketones (b-oh-butyrate, Ac-Acetate): 4 carbon fatty acid
Alcohol: 2-carbon 'the fourth food group' *haa* tequila is paleo, no?

Prior animal pharm: Palmitate Utilized Between Meals




Mitochondrial Medicine

Where does all this high energy production occur? Of course. Your mitochondria (the lower-net-energy anaerobic pathway is independent of mitochondria, occurs in the cytoplasma).

So. Don't scr*w up your mitochondria. That's like jacking your ride. Blowing out your carburetor.

...FLUNKING your human SMOG TEST.

Mitochondrial medicine is a new field but old premises still apply. The paleo evolutionary paradigm for which your mitochondria and DNA were perfected and honed over 2.5M years of natural and sexual selection are what we believe optimize health and maximize vitality.

Apo ε4: Less UV-Triggered Vitamin D Required... Evolutionary Adaptation

** Hat tips to both Mr. Tyler Simmons of Evolutionary Health Systems Blog and a wise, flexible, strong mentor, Mr. Marc Simonson.


The 'Genetic Landscape': Apo E4 Gradient in Europe, China, India and Japan

Mr. Simonson's insights for the migration of pastoralists across Europe, originating from the fertile crescent first started my thinking (nutritional bricolage) for how the world populations have exhibited endless varieties of phenotypes and infinite genotypes (mtDNA, apo E, HFE, and thyroid/autoimmune disorders). He often says that no two people are alike unless they are IDENTICAL TWINS. Therefore, no two dietary prescriptions can be alike.

I'd strongly concur. The perfect human diet is perhaps the one suited to one's ancestral past, unique genomic profile, neolethal toxicity/damage status and metabolic goals.

The below quote comes from Lars Ulrik Gerdes work on Apo E4. He's a FANTASTIC APO*E freak! His thesis is mindblowing. I don't agree w/all of his thoughts but he has plucked through the data comprehensively and thoroughly. Regarding the ApoE4 gradient in Europe (which has also been observed in other countries and continents) 'there is a conspicuous south-to-north gradient of APOE*4 frequencies in Europe, with the proportion of APOE*4 carriers rising from only 10-15% in the south to 40-50% in the north. In contrast, the proportion of APOE*2 carriers is a little higher in Central Europe than in the south and the north. Many other genetic polymorphisms show similar south-to-north gradients in Europe, and this peculiarity of the 'genetic landscape' on our continent is presumably caused by the demic expansion of agriculture (i.e. migrations of farmers) from the Middle East that began about 10,000 years ago. The farmers first migrated westwards along the north coast of the Mediterranean sea, and later turned towards the north. Thus, the APOE*4 gradient could have arisen as an 'admixture gradient', if the apoE*4 frequency were low in the migrating populations of farmers but high in the original populations of hunters/gatherers in the north.'




Evolutionary Adaptation To Lower UV Radiation at Northern Latitudes?

Gerdes has hypothesized that apo E4 allele carriers have less of a need for UV radiation derived vitamin D due to internal adaptations to preserving vitamin blood levels and maximizing intestinal absorption from dietary sources. One of the earliest indications that this was the case was research from Willnow et al. With vitamin D binding protein and apo E protein binding sites being shared regions at the same receptor in the proximal tubule of the kidneys, Gerdes theorized that E4 may have escaped the normal urinary losses of vitamin D and its metabolites. E4 typically produce higher protein amounts of apolipoprotein E (high carb diets lower apo E protein concentrations). From Gerdes' thesis, I restated, see the below. Lard, other pastured animal fats, foraged grub, and organ meats contain substantial, rich sources of fat soluble vitamins including vitamin D. For the ancestral hunter-scavenger-forager 200,000 years ago, these fatty sources of vitamin D, K and A may have been crucial and critical for growth, maintenance and reproduction.

In migrating northward out of sun-drenched Africa, with smaller guts, less fruit/fiber/fish and subsequent lower fermentation of fiber that resulted in SCFA (short chain fatty acids like the potently anti-inflammatory butyrate), how in the world did ancestral HGs survive and have babies?

Upregulation of receptors in the gut for the fat soluble goodies from food and downregulation of the kidney's capacity to leak these fat soluble hormones, metabolites and low molecular weight proteins out...? SUPER HIGH FERTILITY, DIESEL BRAIN FUEL, AND LIPOPHILIC BULLETPROOF IMMUNITY...?

Apo E4, I believe, apparently have ALL of these amazing survivor traits.

Does APOE*4 protect against vitamin D deficiency? [p. 33 from Gerdes' thesis]

A putative association of APOE with bone metabolism has been ascribed to an impact of APOE polymorphism on the transport of vitamin K (see page 40), but it could also relate to vitamin D metabolism and embrace a very strong selection pressure. Hypovitaminosis D in childhood (rickets) causes bone deformations, which can reduce the probability of surviving to adulthood, and perhaps more importantly, can cause pelvic deformations in girls that later may cause their death during delivery under primitive conditions, and also the death of their offspring. Inadequate endogenous production of vitamin D3 can be due to insufficient dietary supplementation or reduced intestinal uptake of the vitamin, or to low exposure to sunlight (UVB-radiation). The latter can be a particular problem to people with dark skin, because melanin blocks for ultraviolet photons and thus limits the synthesis of previtamin D3 [Vogel and Motulsky, 1986].

Mourant and co-workers showed that the frequency of Gc-2-allele for the gene coding for vitamin-D-binding protein (DBP; previously known as the group-specific component, Gc, of the α2-globulins of human plasma) was high in populations living in areas with low levels of sunlight and vice versa (with some exceptions). They suggested that the distribution could be explained by means of natural selection if the encoded isoform were more efficient in binding vitamin, and so in protecting Gc-2 carriers from rickets [Mourant et al., 1976]. This may be true, although the concept has been weakened by an analysis including more detailed climatic data [Cavalli-Sforza et al., 1994].

Interestingly, a very consistent pattern appears if one correlates the frequency of APOE*4 in aboriginal peoples around the world to their skin pigmentation, while also considering the intensity of solar radiation in their habitats:

• The APOE*4 frequency is generally higher in dark-skinned humans than in humans with less melanin, and the frequency is particularly high (40-50%) for instance in Papuans, Pygmies and Khoisan, who are dark peoples and whose (recent) habitats are tropical forests where the intensity of sunlight is relatively low.

• High APOE*4 frequencies (20-30%) are also found in Saami and Inuit, who are moderately pigmented humans living in regions with low average solar radiation, and in peoples living in South American rain forests.

• Conversely, the lowest frequencies of APOE*4 (5-10%) is found among lightly or moderately pigmented humans living in areas of high insolation, i.e. around the Mediterranean Sea, in East Asia, in the southern parts of North America and in Central America.

• The APOE*4 gradient in Europe (and possible also in Japan) could be interpreted to indicate natural selection for this allele with decreasing solar radiation.

The putative advantage of APOE*4 could be related to better intestinal absorption of vitamin D (see page 30), but could also be related, somehow, to the fact that apoE and DBP both binds to megalin. This receptor plays a central
role in vitamin D metabolism, since it binds and internalizes DBP on the luminal surface in the renal proximal tubuli. The function prevents systemic loss of vitamin D through the urine and is also a step in the conversion of 25-hydroxy- vitamin D3 to the biologically active 1,25-dihydroxy-vitamin D3 [Willnow et al., 1999].

Study: Carriers of apo E4 have higher vitamin D (25OHD) blood levels compared to population controls

411 news flash...New research from last month in FASEB supports an earlier speculaton that carriers of the ApoE4 allele require less vitamin D. Willnow's research and Gerdes' theory have a line of evidence for confirmation. To prevent vitamin D deficiency and subsequent health risks (female pelvic dysplasia, fatal childbirths, growth, maturation, steroidogenesis, rickets, testosterone/progesterone production, etc), an evolutionary adaptation to recycling of vitamin D at the kidney level that raises serum vitamin D in apo E4 carriers may have occurred. The researchers state ' The novel link suggests ε4 as a modulator of vitamin D status.'

(Sorry didn't have time for tracking this PDF but if anyone can toss over would be horribly AWESOME *BIG WINK*)

FASEB J. 2011 Jun 9.
APOE {varepsilon}4 is associated with higher vitamin D levels in targeted replacement mice and humans.
Rimbach et al

Abstract
The allele ε4 of apolipoprotein E (APOE), which is a key regulator of lipid metabolism, represents a risk factor for cardiovascular diseases and Alzheimer's disease. Despite its adverse effects, the allele is common and shows a nonrandom global distribution that is thought to be the result of evolutionary adaptation. One hypothesis proposes that the APOE ε4 allele protects against vitamin D deficiency. Here we present, for the first time, experimental and epidemiological evidence that the APOE ε4 allele is indeed associated with higher serum vitamin D [25(OH)D] levels. In APOE4 targeted replacement mice, significantly higher 25(OH)D levels were found compared with those in APOE2 and APOE3 mice (70.9 vs. 41.8 and 27.8 nM, P<0.05). Furthermore, multivariate adjusted models show a positive association of the APOE ε4 allele with 25(OH)D levels in a small collective of human subjects (n=93; P=0.072) and a general population sample (n=699; P=0.003). The novel link suggests ε4 as a modulator of vitamin D status. Although this result agrees well with evolutionary aspects, it appears contradictory with regard to chronic diseases, especially cardiovascular disease. Large prospective cohort studies are now needed to investigate the potential implications of this finding for chronic disease risks.

Vitamin D Dosing Revisited

For those supplementing vitamin D exogenously, care and caution for adverse effects should be monitored. Sunlight derived vitamin D can be shut off -- we have enzymes and systems that control blood/cellular levels, however for supplementation just as taking a birth control or exogenous hormone medication, what goes in, stays in. Previously I listed contraindications for vitamin d supplementation ((a) hypomagnesemia -- get mag up before supplementation because vitamin D will lower serum Mag; (b) sarcoidosis or other condition associated with elevated 25OHD or 1,25OHD3). Now I would add those with E4 should like monitor closely and avoid supratherapeutic levels which probably need to be addressed on an individual basis. With E4 there may be suggestions that intracellular 1,25OHD3 may be higher and this would not necessarily be reflected in serum levels (just like Mag levels are not, intracellular $$$$$ tests are required to accurately assess). Supratherapeutic needs to be individually defined...

So, what's an optimal, ancestral, nutrigenomically perfect serum vitamin D 25OHD and 1,25OHD3 level? I dunno. Who really knows?


Relevant Citations:

LU Gerdes Thesis HERE

The common polymorphism of apolipoprotein E: geographical aspects and new pathophysiological relations.
Gerdes LU.
Clin Chem Lab Med. 2003 May;41(5):628-31.

APOE {varepsilon}4 is associated with higher vitamin D levels in targeted replacement mice and humans.
Huebbe P, Nebel A, Siegert S, Moehring J, Boesch-Saadatmandi C, Most E, Pallauf J, Egert S, Müller MJ, Schreiber S, Nöthlings U, Rimbach G.
FASEB J. 2011 Jun 9.

Essential role of megalin in renal proximal tubule for vitamin homeostasis. Free PDF.
Christensen EI, Willnow TE.
J Am Soc Nephrol. 1999 Oct;10(10):2224-36.

Lipoprotein receptors: new roles for ancient proteins.
Willnow TE, Nykjaer A, Herz J.
Nat Cell Biol. 1999 Oct;1(6):E157-62.

Expression profiling confirms the role of endocytic receptor megalin in renal vitamin D3 metabolism.
Hilpert J, Wogensen L, Thykjaer T, Wellner M, Schlichting U, Orntoft TF, Bachmann S, Nykjaer A, Willnow TE.
Kidney Int. 2002 Nov;62(5):1672-81.

An endocytic pathway essential for renal uptake and activation of the steroid 25-(OH) vitamin D3.
Nykjaer A, Dragun D, Walther D, Vorum H, Jacobsen C, Herz J, Melsen F, Christensen EI, Willnow TE.
Cell. 1999 Feb 19;96(4):507-15.

The uptake of lipoprotein-borne phylloquinone (vitamin K1) by osteoblasts and osteoblast-like cells: role of heparan sulfate proteoglycans and apolipoprotein E. Free PDF.
Newman P, Bonello F, Wierzbicki AS, Lumb P, Savidge GF, Shearer MJ.
J Bone Miner Res. 2002 Mar;17(3):426-33.

Celeb*tchy grrls know their vitamin D and Osteoporosis

Celeb*tchy (ok... where I lurk for laughs...): Gwyneth Paltrow has vitamin D deficiency may develop osteoporosis


Gwen, get some:

1. vitamin D 5000 IU daily in the morning
2. sunshine sans sunscreen

3. vitamin K2 100mcg daily (and/or fermented foods, dairy, CLO)

4. Magnesium (citrate, malate, taurate (since you don't eat much MEAT), chelate, etc) 500-1000mg daily or more

5. BONE BROTH w/grassfed bones + REAL FOOD + FAT D*MN IT

6. Worried, melanoma? Don't. Consume real food/antioxidants proven to prevent UV damage (selenium, iodine, NAC (glutathione presursor), vitamin C + natural E tocopherol, proanthocyanidins (wine/grape seed), pycnogenol, thyroid, maca, plant/animal polyphenols, etc)

7. repeat bone mineral density (BMD) in 2-3 yrs -- will be improved...?normal probably

8. avoid bisphosphonates which make a brittle bone matrix, not crosslinked correctly (like an unstable dense house on sand) -- which are drugs highly linked to spontaneous fractures, poor gum/bone healing, jaw osteonecrosis, inflammation and atrial fibrillation (=strokes/mortality/lifelong-warfarin/etc)
9. lower your serum insulin (basal, postprandial)

10. minerals + hormones: pregnancy leaches minerals and bone-protective hormones (omega-3, vitamin D) vertically to the baby unless mom is totally replete. Birth control especially progestins (ALL) lower bone mineral density compared with placebo (Depo-Provera, the worse, because injected; pellets and IUD and orals, TOTALLY bone degrading)

***Comments crack me up from: cheekemunkey, MightyMouse (no it's not me, I'd be batgrrrl) *haa aha*

Sounds like evo/paleo hunter-gatherer grrrrls.


Peter initiated... *haa*



Hyperinsulinemia and Metabolic Syndrome (which is a high insulin syndrome) are highly associated with bone degradation, bone fractures and osteoporosis. Consider also a grain-free, soy-free, lower carbohydrate diet... to prevent trigging all that insulin that grows inflammatory belly fat which breaks down bone.



Osteoporosis Resources:

o The Standard, Guilliam PhD

o Vitamin D 5000 IU daily normalizes 25OHD PTH in 12 months and improves BMD as good/better than a bisphosphonate (thanxxx Neo!)

Healthy bones [and clear arteries without calcifications, see Rotterdam and HERE] require as evident in this recent study:
--25OHD ~50 ng/ml
--PTH < 20 pg/ml

--[optimal thyroid (TSH FT4 FT3 rT3) -- not discussed, important and ultimately vital for the intimately inter-related network of endocrine organs: parathyroid, thyroid, kidneys, adipose, gonads, marrow... B-O-N-E-S ]



Evolutionary Medicine posts (Dr. Tourgeman):

(1) Brain, Bone and Metabolism (2) Celiac Disease and Osteoporosis; (3) Drugs That Weaken Bone Structure

'Roid Rage: Vitamin D3 -- DO IT (Part II)

Vitamin D and Athletes

Vitamin D is not just a sun-derived vitamin, but is a crucial steroid precursor that is transformed into one of the most potent hormones in the human body for strength, power, lung function and regulating gene expression in every organ system.

Athletes need Vitamin D.

Dr. Cannell has written quite extensively about the role of vitamin D in athletes.

See prior post: 'Roid Rage Vitamin D3 -- DO IT (Part I)



Don't miss Dr. T's recent post: Vitamin D Summary of Actions. SUPERB!




Vitamin D: Flu, Asthma, Bronchitis, H1N1 Protection

Swine Flu H1N1.

Worried? Don't be.

Baby wanna be a millionaire? Vitamin D3... just do it. Baby by me, 50 cents YO.


Many factors can predispose an individual to be immunocompromised and more susceptible to the flu or H1N1 or bronchitis:
--sleep deprivation
--mental stress
--excessive physical training
--fatigue
--hypothyroidism, adrenal fatigue
--VITAMIN D INSUFFICIENCY
--VITAMIN D DEFICIENCY
--poor, unbalanced gut biofilms (read Dr. Ayers Cooling Inflammation)
--gluten/wheat, lectins, omega6 and associated inflammation
--nutritional deficiencies
--et cetera


Vitamin D stores may be depleted under all the circumstances above.

For the past season, naturally, I've been a total ding dong, frequently skipping my vitamin D supplement and sunlight. Yeah missed a boatload of doses. (*haaa* Yeah, I am THE vitamin-D-fairy-godmother and I hand it out like candy... wtf I s*ck) So... Three weeks ago my asthma came back full force and within days I was in the middle of a bronchitis/coughing attack again with a fever for 2 days. Last episode was EONS ago. Couldn't shake it but after a boost of vitamin D via a modified Stoss protocol (20,000 to 50,000 IU for 3 days) that Dr. Cannell frequently discusses for prophylaxis or acute treatment of influenzae or other viral infections, my coughing and infection were completely gone. My cough was almost gone OVERNIGHT. On the other hand, Dr. Cannell talks about much higher doses. Since I was not deficient, just 'insufficient', I used a lower dose.

The bronchitis was entirely aborted, shortened to a few days not a few MONTHS or a few WEEKS like the normal course of chronic bronchial inflammation I had experienced annually in the past. I ran 13.1 miles a week later and was fine (though my power and pace s*cked). My ghetto batgrrrl picture wasn't so bad though *wink*. Vitamin D does a body better. My skin, hair, muscles, recovery, breathing and body fat are all far better now that I'm back on the program.

Prior post: Stoss protocol Vitamin D3 Nature's Antibiotic

Vitamin D deficiency and chronic lung disease. Gilbert CR, Arum SM, Smith CM. Can Respir J. 2009 May-Jun;16(3):75-80.

Vitamin D and respiratory health. Hughes DA, Norton R. Clin Exp Immunol. 2009 Oct;158(1):20-5. Review.




Vitamin D Associated with Fitness, Power, Strength and Lower Body Fat

Two research articles highlight the relationship between higher vitamin D levels and athletic performance. The first showed a positive relationship between higher VO2 max and higher blood vitamin D (p<0.05) in n=59 adolescent and young females. Incidentally, lower body fat (p<0.05) was associated with higher vitamin D levels.

The second study reviewed baseline vitamin D concentrations (which were LOW low low) in 99 female athletes age 12-14 yo and found "Jumping mechanography to measure muscle power, velocity, jump height, and Esslinger Fitness Index from a two-legged counter movement jump and force from multiple one-legged hops was performed. Body height, weight, and serum concentrations of 25(OH)D, PTH, and calcium were measured. RESULTS: Median serum 25(OH)D concentration was 21.3 nmol/liter (range 2.5-88.5 [median 8 ng/ml with range 1-35.4 ng/ml]) and PTH 3.7 pmol/liter (range 0.47-26.2). After correction for weight using a quadratic function, there was a positive relationship between 25(OH)D and jump velocity (P = 0.002), jump height (P = 0.005), POWER (P = 0.003), Esslinger Fitness Index (P = 0.003), and force (P = 0.05). There was a negative effect of PTH upon jump velocity (P = 0.04). CONCLUSION: From these data we conclude that vitamin D was significantly associated with muscle power and force in adolescent girls."


Girl Power!

Association among cardiorespiratory fitness, body fat, and bone marker measurements in healthy young females.
Mowry DA, Costello MM, Heelan KA. Mowry DA, Costello MM, Heelan KA. J Am Osteopath Assoc. 2009 Oct;109(10):534-9.

Vitamin D status and muscle function in post-menarchal adolescent girls.
Ward KA, et al. J Clin Endocrinol Metab. 2009 Feb;94(2):559-63.




Vitamin D Alters Gene Expression

Many components of our diet are in fact potent modulators of genetic expression. Vitamin D is among many. In a variety of clinical trials, vitamin D lowers CRP (inflammation), increases testosterone (I've seen it and HH reports his anecdotal experience here), thyroid hormone, and (in rats) raises estrogen. Is this helpful for athletes? There are many mechanisms by which vitamin D exerts benefits for athletes including improved breathing, lung function, oxygenation, immunity protection, muscle strength, endurance, muscle power and hormone optimization (e.g. the big 'T').

Micronutrients and amino acids, main regulators of physiological processes. Verheesen RH, Schweitzer CM. Med Hypotheses. 2009 Oct;73(4):498-502.

Human physiology is supposed to be a complex interaction of regulating processes, in which hormones, genes, their proteins and apoptosis are thought to play a dominant role. We hypothesize that regulation of physiological processes is mainly influenced by amino acids and micronutrients with hormones, proteins, apoptosis and gene modifications being their derivatives. Furthermore, we suppose that the cells power plant, the mitochondrion, is in fact an intracellular bacterium, living in absolute symbiosis. Because of its intracellular existence it depends on the host's micronutrients completely. Within the host these micronutrients regulate their own formation, degradation, uptake and excretion. Known deficiencies, such as iodine and vitamin D, affect billions of people. Many micronutrients neither have been investigated, nor have they been studied in relation to each other and solid data are not available. Optimal levels of many micronutrients and all amino acids are not known.

Amino acids, vitamins and minerals are capable of altering gene expression, inducing apoptosis and regulating chemical processes. It makes them highly attractive for creating better health, against low cost, as we have already proven in the case of rickets, cretinism and scurvy in severe deficiencies. By creating optimal living conditions and study mitochondria from a symbiotic point of view we suppose that diseases not only can be prevented, but the course of diseases can be altered as well.

Ask Your MD for A Blood Test

Tracking of blood vitamin D levels (known as [25(OH)D]) is necessary to make sure you have the optimal range, not too high and not too low. Other labs to track are calcium and magnesium (and PTH if you have plaque or chronic kidney disease). Supplementation with either over-the-counter Vitamin D3 or prescription ergocalciferol (which is inferior and should be avoided) is contraindicated if you have a condition called sarcoidosis or isolated hypercalcemia (high calcium).

With dose initiation or increases, the blood levels take about 4-6 wks to stabilize. Consider requesting a blood test to confirm the value (either self-directed ZRT at heartscanblog or the vitaminDcouncil.org).

Dr. Harris MD discusses the accuracy of the vitamin D tests available on the market. Don't be blinded by his scorching hot brilliance or body. Paleo nutrition blog: HERE and HERE.

Dr. Cannell MD advises goal serum vitamin D [25(OH)D] 60 to 80 ng/ml (or 150-200 nmol/L). Personally my breathing and hormones appear to me the most optimal at 70s ng/ml. The past year I checked the [25(OH)D] twice and it was not more than 60. Incidentally, I did not feel so 'right on' as compared to when I had levels in the 70s. Everyone perhaps owns a 'set point' and you might need to figure what that is for yourself depending on your athletic performance, pulmonary function, immunity, mood and other metrics.

Hopefully your doc will not ignore the healing power of diet and certain nutritional supplements like vitamin D. (bwt don't bring the below article in -- the suggested doses are pathetically low baby doses).

• Nutrition 101: physicians can no longer ignore the healing power of diet and nutritional supplements. O'Keefe JH. Expert Rev Cardiovasc Ther. 2008 Jun;6(5):593-6.PDF here.

Low Vitamin D = Low Strength

Low serum Vitamin D concentrations are independently associated with SARCOPENIA decreased muscle strength:

• Concomitant lower serum albumin and vitamin D levels are associated with decreased objective physical performance among Japanese community-dwelling elderly.
  Kwon J, Suzuki T, Yoshida H, Kim H, Yoshida Y, Iwasa H. Gerontology. 2007;53(5):322-8.
• Relationship between muscle strength and vitamin D metabolites: are there therapeutic possibilities in the elderly?
  Bischoff HA, Stähelin HB, Tyndall A, Theiler R.
  Z Rheumatol. 2000;59 Suppl 1:39-41.
• Prevalence of sarcopenia and predictors of skeletal muscle mass in healthy, older men and women.
  Iannuzzi-Sucich M, Prestwood KM, Kenny AM.
  J Gerontol A Biol Sci Med Sci. 2002 Dec;57(12):M772-7.
• Effects of vitamin D supplementation on strength, physical function, and health perception in older, community-dwelling men.
  Kenny AM, Biskup B, Robbins B, Marcella G, Burleson JA.
  J Am Geriatr Soc. 2003 Dec;51(12):1762-7. [Vitamin D 1000 IU daily was not sufficient to statistically improve strength or perception]

Cardio Controversies: Tale of Two Equal LDLs and 17-fold MI Risk

Figure 2. Cox proportional hazards survival curves demonstrating
time to acute MI for patients with a yearly calcium volume
score change > 15% or < 15%. Callister et al, 2004 ATVB.

TITLE: Progression of coronary artery calcium and risk of first myocardial infarction in patients receiving cholesterol-lowering therapy.

Free PDF click HERE. Raggi P, Callister TQ, Shaw LJ. Arterioscler Thromb Vasc Biol. 2004 Jul;24(7):1272-7.

OBJECTIVE: Statins reduce cardiovascular risk and slow progression of coronary artery calcium (CAC). We investigated whether CAC progression and low-density lipoprotein (LDL) reduction have a complementary prognostic impact.

METHODS AND RESULTS: We measured the change in CAC in 495 asymptomatic subjects submitted to sequential electron-beam tomography (EBT) scanning. Statins were started after the initial EBT scan. Myocardial infarction (MI) was recorded in 41 subjects during a follow-up of 3.2+/-0.7 years. Mean LDL level did not differ between groups (118+/-25 mg/dL versus 122+/-30 mg/dL, MI versus no MI). On average, MI subjects demonstrated a CAC change of 42%+/-23% yearly; event-free subjects showed a 17%+/-25% yearly change (P=0.0001). Relative risk of having an MI in the presence of CAC progression was 17.2-fold (95% CI: 4.1 to 71.2) higher than without CAC progression (P<0.0001). In a Cox proportional hazard model, the follow-up score (p=0.034) as well as a score change >15% per year (P<0.001) were independent predictors of time to MI.

CONCLUSIONS: Progression of CAC was significantly greater in patients receiving statins who had an MI compared with event-free subjects despite similar LDL control. Continued expansion of CAC may indicate failure of some patients to benefit from statin therapy and an increased risk of having cardiovascular events.
PMID: 15059806



Cardio Controversies: Dr. Callister MD

I think Callister is cool. First he found statins were associated with regressed EBCT scores in 1998 but then confessed up when he could not replicate it in several subsequent trials. He has even postulated why. Correctly I think!

He and his colleagues have found a dilemma in current cardiology concepts, much like Dr. Superko. Despite LDL < 120 mg/dl and treatment with statins, patients progressed to an MI when the calcium volume score via EBCT increased > 15% annualized. In fact, they summarize that "the relative risk of suffering a MI in the presence of CVS progression was 17.2-fold (95% CI4.1 to 71.2) higher than that of subjects without progression (P<0.0001)."

Our goal at TYP as designated by Dr. Davis from his extensive experience and research is for EBCT annualized progression of no more than 10% to halt all risk of long-term clinical CAD events. Naturally, some EBCT regression is desirable.



Is LDL Reduction Necessary?

For reduction in hard clinical events, is LDL reduction really necessary? Actually, I don't think so... From lipid researchers like Dr. Barry Sears PhD on omega-3 and the tremendous outcomes from the secondary prevention Lyon Heart Diet trial, we know that with a significant reduction of dietary omega-6 toxic vegetable oils and sufficient increments of dietary omega-3 (ALA, EPA, DHA), clinical CAD events can be nearly halted in very high risk group of CAD individuals. Moreover, with only minor improvements in the n-6:3 balance a reduction in all-cause mortality (cancer, suicides, accidents, etc) in addition to CAD mortality and events was observed in this landmark study. Recall, these improvements were witnessed with no improvements in total HDL (final 49 mg/dl) or LDL (final 161 mg/dl). I always have to ask why save the heart and coronary vessels yet advance to experience cancer and/or suicide and depression? One of the most tragic and saddest stories that I have come across related to the low-saturated fat debacle is that of the famous Dr. Pritikin who conquered heart disease but committed suicide after silently battling leukemia. What was he missing? Could his demise have been prevented?



Low Dietary Saturated Fat

Why may low saturated fat be dangerous for the long-term? Can a 'deficiency' in dietary saturated fat be as insiduous and quietly dangerous as cancer or subclinical atherosclerosis itself?

I see a lot of HDLs in the 20s 30s 40s (or HDL2b nonexistent to single-digit). What is wrong with these kind of numbers? For one, according to clinical trials, they are highly associated with CAC progression and early events. Of course, there are cases that are exceptions to the rule... for instance if you are . . .
(1) Nissen infusing HDL-apoAI-recombinant pieces into your arm every night (JUST KIDDING... don't get any stupid ideas)
(2) an apo A1-Milano carrier
(3) allergic to kryptonite *haa*
(4) consuming boatloads of niacin or omega-3 fish oil until gills grow


Are low HDLs a sign of dietary saturated fat deficiency? Or just high carbohydate intake? Or both? Moreno JA et al showed that with a high fat diet (40%) both high saturated fat (20% SFA) and high monounsaturated fat (22% MUFA), shifted individuals equally from pattern B to A when compared to a high carbohydrate (CHO 57%) diet (J Nutr. 2004 Oct;134(10):2517-22). PDF click HERE. However, like other saturated fat studies, only the SFA diet across every apo E type (4/3, 3/3, 3/2) raised the HDL to the highest degree. Interestingly, apo-AI was increased as well to the greatest magnitude with the high saturated fat diet and was the case for every apo E genotype. Both HDL and apo-AI are atheroprotective and associated with plaque regression. See below chart (p<0.05). FYI, these diets in healthy volunteers were still very VERY high carbohydrate at (yikes) 47% and explains why a higher majority of individuals were pattern B (predominance of small dense atherogenic LDL) to begin with, particularly in the males. Certainly, I know I would immediately be clinically T2DM with this type of diet.





Callister's Other Findings: 'Incomplete Effectiveness of Statins'

Callister et al concluded that 'statin resistance' may be responsible for the lack of efficacy for these drugs in preventing hard clinical events observed in this trial. How about...

Lack of HDLs?

Excessive carbohydrates? 47+% Carbohydrates in the AHA 'low fat' diet?

Lack of dietary saturated fatty acids?

The authors concluded that "molecular mechanisms—as yet not fully understood—could help explain the incomplete effectiveness of statins therapy. The HMG-CoA reductase enzyme is a pivotal rate-limiting enzyme in the production of intracellular cholesterol and is selectively inhibited by statins. To inhibit excess synthesis of cholesterol, the HMG-CoA reductase enzyme is degraded in the presence of high levels of intracellular mevalonate and sterols. Statin resistance at the cellular level has been described to occur via 2 mechanisms: overexpression of the gene regulating secretion of the HMGCoA reductase enzyme and loss of degrading ability of the enzyme in cell cultures exposed to high concentration of lipoproteins and lovastatin in the medium."


OK... well they were close. HMGCoA reductase is certainly controlled by several factors. Ness and Chamber discuss this 'cholesterol buffering capacity' effect of HMGCoA reductase, the enzyme that produces LDL-Cholesterol (the good lbLDL and the 'bad' sdLDL) and is mechanistically inhibited by statins. Unfortunately like all interconnected systems in biological environments, feedback control ultimately inhibits or stimulates HMGCoA reductase activity based on many factors which are regulated by needs for growth, reproduction, fasting v. fat-storage, and relaxation. Click HERE.
--dietary cholesterol downregulates (yup... cheap-egg-yolks vs. Crestor; yolks WIN)
--hyperinsulinemia turns it on (poor glycemic diabetic control, high-carbs-low-fat-idiocy, again)
--hypothyroidism turns on
--peri- and menopause (low estrogen states -- or like those induced by $*%&@# contraceptives and $*%&^! progestins)
--high cortisol (mental stress, physical stress)
--lack of bile salts (taurine deficiency)




Factors NOT Affected by Statins: Lp(a), IDL, Small LDL, Microbes

Callister and the other authors are brilliant! In addition, they concluded: "Because we did not measure hemoglobin-A1c, we were unable to verify whether the glycemic control had an effect on CVS progression and development of MI. Lipoproteins not affected—or incompletely affected by therapy with statins—such as Lp(a), small dense LDL, and other mediators of vascular damage (viruses, homocysteine, fibrinogen, Chlamydia Pneumoniae, and others) may also have played an important role that could not have been detected because of the design of our study."



What Does Lower Lp(a), IDL, Small Dense LDL and Microbial Burden?

Oh please... Gentle Readers... I hope you get this correct.

Yes?

Saturated fatty acids, my dear audience members, of course.

Synergistically with a low LOW carbohydrate diet (or no carb).

Did you know that coconut oil, grassfed ghee/butter, cream, tallow, lard (which contain short-, medium- and long-chained saturated fatty acids) control and kill yeast, parasites and other microbes like Giardia, Salmonella and Campylobacter, in vivo and in vitro?



Krauss is in the House! The Three Axes of Evil

Yes -- of course (without Superko's help) Krauss has figured it out again and confirm the theories above as well as what we already acknowledge and tackle at TrackYourPlaque. Subfraction of lipoproteins yields the 'death' bands on ion mobility analysis which are independent subsets of cardiovascular risk. (Krauss et al, Arterioscler Thromb Vasc Biol. 2009 Sep 3. Not free yet.)

(PC1) LDL-associated risk: Concentration-sdLDL, Small Dense LDL, VLDL [Lipoprotein (a)]

(PC2) Metabolic Syndrome/Hyperinsulinemia pattern of decreased large HDL, increased small/medium LDL, and increased triglycerides (eg, Pattern B)

(PC3) HDL-associated protection: large HDL subfraction ('absent' band)

Note: Krauss does not list Large LDL-P as one of the axes of coronary risk. After reviewing 3 large landmark trials, he and the other researchers concluded Large LDL are not associated independently with CAD risk. Again, the presence of small LDL-IVb (the densest of 7 subparticles) is associated with risk and progression of plaque, not a high particle count of Large LDL.

Krauss and the other authors state, "Our study demonstrated that (1) levels of small/medium LDL particles are associated with [CV disease] and (2) levels of large LDL particles are not significantly related to cardiovascular disease, is consistent with other large prospective cohort studies whose data were obtained by 2 different lipoprotein measurement techniques: the Quebec Cardiovascular Study (GGE) and the Multi-Ethnic Study of Atherosclerosis and Women's Health Study (NMR). (p. 5)"

Large-LDL are Not Associated with Increased CAD Risk

This bears redundancy. Many cardiologists and even NMR experts do not understand this concept. Repeat... Krauss and other cardiologists found no increased risk associated independently with the presence of Large LDL.

Why is Large LDL even implicated sometimes?

Are fire-fighters implicated in causing atrocious out-of-control fires?

No. That is frankly ridiculous...

The arsonist is the smallest densest LDL. (See PC1 or PC2.)
And, the co-conspirator is the lack of large HDL2. (See PC3 or PC2)


(Read: dietary saturated fat deficiency. Excessive compliance with the AHA low chol/sat fat indictment).

Genetically we are all different -- some individuals naturally produce more Large LDL (apo E4? these folks elude infectious agents better, esp coupled with Lp(a); unfortunately the CAD is concordantly worse on inappropriate diets, e.g. non-ketogenic). However, when the NMR is examined, these individuals who have both CAD and bunches of Large LDL exhibit the 'death' band. Subfraction particles of LDL-IVb will often be 10x higher than normal. Or even 20x higher. What's normal and optimal? Optimal is none to 0.60% in my opinion.




Pattern A + the tiny LDL-IVb 'death' band is not a good thing.

You only need one axis of 'evil' for heart disease and EBCT progression.

Paleo folks sometimes have very high LDL mass and stunningly enormous proportions of Large LDL. Funny... this is also observed in individuals in longevity and centenarian studies. The long-living 100-year old Ashkenazi Jewish (pro-bands) have enormous HDL and Large LDL yet the small dense LDL was minor consisting of ~6-7%. Is all that Large LDL harmful? I doubt it. Their offspring have HDLs like us mod-high fat Paleo folks of 80s-100s. Okinawan centenarians also have enormous HDL of 60s with consuming goat milk full of saturated fat (MCTs), lard, fatty pork and gamey goat sashimi. Their LDLs are high in the 100-120s mg/dl like the Ashkenazi.

Read here: Benefits of High-Saturated Fat Diets (Part II).

For the Paleo/Primal/PP folks, if the LDL is mostly (or all) large, no problem. If however there are some of the smallest densest stuff (subspecies: LDL-IVb, the black sheep) and no large HDL2, then... it... maybe a problem. LDL-IVb is eradicated within 4wks with the right diet. Low low carb, fat and protein, Paleo.

Only subfractionation of the lipoproteins will identify the culprit.





Statins Fail to Improve ALL 3 Principal Components (PC)

Do statins help with any other of the above independent axes of coronary risk: PC1, PC2, or PC3? Or other identified CAD risk factors: vitamin D deficiency? Omega-3 deficiency? Hypothyroidism? Excessive omega-6 clogging up cell membranes and raising serum insulin and inflammatory markers?

Well... statins raise vitamin D. (yeah... Sunshine/ supplement v. Crestor which raises vit D 159%? Sun+Vitamin D WIN. When my blood [25OHD] increased from 20 to 70 ng/ml (350%), my HDL increased 29%. OK... here is a vitamin D formula: every 10% vitamin D conc increase = 1% HDL increase; according to Castelli, every 1% HDL increase is equivalent to 2-3% CAD relative risk reduction)


Well...statins may raise HDL max 5-15% yet niacin raises HDL 30-200% (depending on duration and patient population).

So the action on promoting regression via HDL by Niacin is 2 to 40x more than statins.

Niacin prominently lowers Lp(a), small dense LDL/IDL, triglycerides and provokes shifts to Pattern A. In the HATS trial, recall, after 3 yrs, niacin raised HDL 30% and HDL2 60%. Niacin was associated also with reductions in blood pressure. Statins are not in any trial.

In fact, any non-synthetic, therapeutic intervention that raises HDLs also lowers Lp(a), IDL, small dense LDL/medium LDL and triglycerides. And increases nice large buoyant LDL. Indeed, these lipoprotein species all improve in parallel. Conversely, they are exacerbated in parallel. With no exception, any strategy that raises HDLs consequently affects blood pressures positively downstream (eg, carb restriction, body fat loss, lean muscle gain, yoga, omega-3, vitamin D, saturated fat intake, thyroid replenishment, hormone optimization, many antioxidants and proanthocyanidins).

Except statins. What the authors missed mentioning was that in addition to 'statin resistance', statins worsen Lp(a) and Percent-sdLDL. And they fail to shift to pattern A. What else?
Statins s*ck.



Correctly Catching the Calcification Culprit(s)

TrackYourPlaque is a self-management program. To optimize the program and control plaque, one must accurately and knowledgeably assess personal and familial risk factors that caused suboptimal lipoproteins and/or positive EBCT scores and progression. The three factors listed above comprise 99% of the most common coronary culprits.

If one is just trying to beat down the LDL-Particle Count into submission and fails to take into account the three 'axes' of coronary risk, one will invariably miss the big picture.

Is it... dangerous...??

Certainly... it is not equivalent to EBCT stabilization or regression. Targeting and ameliorating the correct coronary culprits on the other hand yields potent control on plaque and reduce EBCT calcification progression to < 10%. For regression in 9-18 months on EBCT, 'perfect' lipoproteins are not mandatory but a trend toward improvements in both reductions in small dense LDL, IDL, Lp(a) and increases in HDL2 and relative LDL-buoyancy are requirements. Control of hypertension, more vitality, loss of body fat are all extra side perks.

Do you have 'leaky gut' where microbes are flowing into the blood stream from the intestines?
Do you have low HDL?
Do you have high small-LDL?
Do you have Pattern B?
Do you have Lp(a) and/or high homocysteine?
Do you have progression or calcium score > 10% annualized?
Do you have premature CAD or stroke or peripheral vascular disease or renoarteriosclerosis in your family history?
Do you have proteinuria, dialysis or chronic kidney disease in your family?
Do you have heart failure in your family history?
Do you have 'statin resistance'?

Then... one cannot hesitate or prolong an approach that is more targeted and aggressive than the one that Callister and his colleagues discussed ('incomplete effectiveness') associated with a 17.2-fold MI-risk in 6-7 years.


Ketosis/niacin, low LOW carb Paleo diets, mod-high SFA diets, high omega-3 supplementation, dietary omega-6 elimination, hormone optimization, cardio/weights and many MANY other TrackYourPlaque strategies improve all three axes of high cardiovascular risk.



Related posts:

Egg Yolks and High SFA Diet Raise HDL2, Lower IDL VLDL triglycerides, and Increase LDL Particle Buoyancy

Benefits of High-Saturated Fat Diets (Part I): Krauss 18%-High SFA Diet Lowers sdLDL particularly LDL-IVb, Raises HDL2b and lowers IDL VLDL triglyerides

Benefits of High-Saturated Fat Diets (Part III): High SFA, Low Carb Paleo Diet annihilate sdLDL from 1000nmol/L to nearly no particles or 'None', Raises both HDL2/HDLs 200-400%, Lowers IDL VLDL triglyerides, Lowers Lp(a)

HDL2b: Quintessential Regression Particle and How to Raise It

Lp(a) and Women's Heart Risk

Umbellularia Californication: SFA kicks olive oil's *ss

Lp(a) and the Power of Fish Oil (8.5 grams/d EPA DHA)

Vitamin D: Disease Prevention

Image: courtesy of grassrootshealth.org (and imminst.org)




Cancer and Vitamin D
Few prospective vitamin D trials exist in the literature in humans for cancer. Our best data exists as epidemiological observations. The above wonderful graphic depiction of the relationship between disease prevention and serum concentrations of vitamin D [25OHD] was complied by grassrootshealth.org. Dr. Davis attended a conference last year and learned that the NIH budget for studying cancer and vitamin D will be increased by $200 million. Heartening to know that funding is being put to actually good use. Cancer has now superceded heart disease to take the #1 spot for mortality in the U.S. Hopefully we'll learn more in a decade or a two! I believe it is difficult to expect Pharma or other large deep-pocketed research giants (backed by lobbyists) to fund a trial where the preventive treatment (OTC at Trader Joe's or Walmart or Target or Costco or iHerb.com) costs as little as $2 per month and prevents a $150,000+++ cancer treatment paid for by Medicare and most insurance companies.

In the meantime...can you afford to wait for the research results?

Hopefully NIH scientists will 'get it right'... and...
(1) Use the therapeutic doses of vitamin D 4000-8000 IU daily (not 400-800 IU daily which are literally doses recommended for babies, infants and toddlers by the Academy of Pediatrics),
(2) Use vitamin D3 (not synthetic D2 which is not metabolized well by majority of the globe, esp Indo-Asians, and is linked to toxicity compared to natural D3)
(3) Use 'tracking' of [25OHD] blood concentrations
(4) Use results where [25OHD] is greater than 50 ng/ml (not just greater than 30 ng/ml... see above graph). [25OHD] of 30 ng/ml accomplishes nearly N O T H I N G... except rickets prevention greater than 99%.


Don't you deserve greater than 35%, 83%, 17%, 60%, 18%, 66%, 50%, 72%, 54%, 30%, 49%, 37% prevention, respectively for the cancers and conditions listed above?

And your family and friends?




Vitamin D, Safety and Dosing
Dosing depends on a variety of factors. You really don't know if you have the right dose unless you check 4-6 wks after initiating supplementation. Everyone is uniquely different and so are the enzymes which activate and de-activate vitamin D and its derivatives, the skin protective melanin/pigmentation which blocks excessive activation, how much time spent indoors, how much makeup/sunscreen/clothes are worn, etc.

Dr. Cannell, Dr. Davis and other vitamin D experts advise starting at vitamin D3 5,000 IU daily in the morning/daytime if you receive no sunlight or live in an area devoid of UVB radiation (~half of the year nearly zero UVB above the 37th latitude).

The below graph is from a prominent vitamin D researcher, Dr. Vieth, in Canada where vitamin D supplementation is nearly mandatory (Vieth R 1999). I've superimposed the dose I take to achieve 60 - 70 ng/ml, vitamin D 5,000 IU daily. In winter I take 8,000 to 10,000 IU daily which is more similar to the dosing curve Vieth has determined in his clinical research.

For U.S. standard lab values, to convert nmol/L to ng/ml, divide by 2.5.

Dr. Vieth writes that "The clinical trial evidence shows that a prolonged intake of 250 mug (10,000 IU)/d of vitamin D(3) is likely to pose no risk of adverse effects in almost all individuals in the general population; this meets the criteria for a tolerable upper intake level (Vieth R 2007)."



FIGURE:
Dose response for vitamin D intake versus final serum 25-hydroxyvitamin D [25(OH)D] concentration reported. Circles indicate group means from Tables 4 and 5. Points indicated by "X" represent single values from Table 5 for people reported as intoxicated with vitamin D. The arrow indicates the lowest dose reported as causing hypercalcemia, but which is an outlier because vitamin D was given as a single dose of 7500 µg (300000 IU)/mo, instead of 250 µg (10000 IU)/d (77). If authors reported 25(OH)D for several time points, only the final serum 25(OH)D is shown in the figure. The line representing the dose response passes through the points that represent group data.


Low wintertime vitamin D levels in a sample of healthy young adults of diverse ancestry living in the Toronto area: associations with vitamin D intake and skin pigmentation.
Gozdzik A, Barta JL, Wu H, Wagner D, Cole DE, Vieth R, Whiting S, Parra EJ.
BMC Public Health. 2008 Sep 26;8:336.

Vitamin D from dietary intake and sunlight exposure and the risk of hormone-receptor-defined breast cancer.
Blackmore KM, Lesosky M, Barnett H, Raboud JM, Vieth R, Knight JA.
Am J Epidemiol. 2008 Oct 15;168(8):915-24. Epub 2008 Aug 27.

Evidence for genetic regulation of vitamin D status in twins with multiple sclerosis.
Orton SM, Morris AP, Herrera BM, Ramagopalan SV, Lincoln MR, Chao MJ, Vieth R, Sadovnick AD, Ebers GC.
Am J Clin Nutr. 2008 Aug;88(2):441-7.

Vitamin D toxicity, policy, and science.
Vieth R.
J Bone Miner Res. 2007 Dec;22 Suppl 2:V64-8. Review.

Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety.
Vieth R. PDF here.
Am J Clin Nutr. 1999 May;69(5):842-56. Review.

Raving/Raging More On Vitamin D: DOSING

Once people start on appropriate doses of vitamin D... And...I am not referring to LICKING A CAPSULE, they come up to me and tell me HOW GREAT THEY FEEL.

More energy, more vitality and feeling younger.

In only o n e w e e k. Wowo.


Vitamin D is certainly a steroid precursor which has benefits for everyone. Not just athletes.



Who Frequently Needs Higher Doses?

I've broken this down to a few subgroups from my experience:
--Leaky gut (these benefit highly from the protective/healing effects of probiotics+digestive enzymes combined)
--Morbidly obese (but not necessarily)
--Again, those with leaky gut -- those still consuming WHEAT (and/or casein if sensitive)
--Genetically those who may be fast-metabolizers. Who r u? I have no idea. Ck your blood levels and if it does not respond in 6-8wks, you may be one of them. Hx Rickets? Hx Grave's? Hx Hashimoto's??
--Drugs which increase metabolism, disposal, elimination of fat-soluble drugs, xenobiotics and VITAMINS ADEK omega-3s EPA DHA -- anti-seizure drugs Valproic acid, Depakote, Carbamazepine and others incl Calcium channel blockers
--Those taking stupid drugs like Xenical or ALLI which block fat absorption (or ?Zetia as well hypothetically)




Contraindications to Vitamin D Therapy

If your blood levels of 1,25 OHD (calcitriol, one of the active metabolites) or 25-OH-D (calcidiol, another active metabolite) are fine or elevated, then you don't need supplementation.
--Plenty of sunlight exposure (esp equatorial, esp midday, esp when "your shadow is shorter than you are" per Dr. Cannell)
--Frequent naked *winky*, clothes-less, makeup-less, sunscreen-less exposure
--Dialysis patients already taking Rx Calcitriol where blood levels are optimal which they hardly ever are. Current national DOQI guidelines are to include Vitamin D supplementation and to achieve 25OHD blood concentrations appropriately.


Who should absolutely not receive supplementation?
--Sarcoidosis (already high calcitriol from inappropriate secretion secondary to autoimmune proliferative changes)
--Some weird malignant cancer where the cells are overproducing either calcitriol or calcidiol



Dosing

No... 100 IU Vitamin D from a cup of casein-milk will not get anyone ANYWHERE.

Babies from Day One are advised now from the Academy of Pediatrics to receive orally 400 IU daily (this is DOUBLE from prior recommendations of 200 IU daily) either from supplementation drops, formula (1-2 cups daily? wtf), or Momma's milk (if Momma chooses to improve her baby's health to supplement herself since 99% of Momma's are ALL also deficient).

Clover Organic Farms Milk
(reduced fat, whole, or nonfat)
Vitamin D3 content = 100 IU (25% of RDA) in one cup = 8 oz




Why Milk Even Contains Vitamin D

For the treatment of rickets in the early 1900's, the U.S. mandated vitamin D 400 IU to be added to every quart of milk (4 cups).

Let's say my minimal requirement for vitamin D is 5000 IU, barring any UVB exposure where typically a human would receive 99% of vitamin D sources (food provides less than 30-100 IU per serving like dairy, fish, liver, caviar or otherwise).

I would have to drink 50 (eg, F I F T Y) cups of milk to provide what my growing (ghetto fab/PHAT/HAWT) body would need...


FIFTY.


Milk isn't even Paleo.

Milk... Don't do it.

BTW...Casein, one of the main proteins in dairy sources, has been linked to many autoimmune disorders in susceptible folks (eg, autism, ADD, MS, Hashimoto's, RA, Sjogren's, Migraines, Type 1 Diabetes, Uveitis, IBD, Cholangitis, NASH/Liver Cirrhosis, etc). ??? CAD probably too.
Range of neurologic disorders in patients with celiac disease.
Infections, toxic chemicals and dietary peptides binding to lymphocyte receptors and tissue enzymes are major instigators of autoimmunity in autism.
Intestinal lymphocyte populations in children with regressive autism: evidence for extensive mucosal immunopathology.
Collagen disease: the enemy within.
Possible immunological disorders in autism: concomitant autoimmunity and immune tolerance.
Enterococci in milk and milk products.(and migraines)
[Cerebral calcifications: a clue for a diagnostic process in a nonspecific clinical case] (migraine)
[Primary headaches and the influence of inflammatory diseases of the CNS and their respective immunmodulatory therapy]
The neurology of gluten sensitivity: separating the wheat from the chaff.
Antibodies to bovine beta-casein in diabetes and other autoimmune diseases.
Cell-mediated immune responses to GAD and beta-casein in type 1 diabetes mellitus in Thailand.
Autoimmune uveitis and antigenic mimicry of environmental antigens.
Serum antibodies to cow's milk folate-binding protein in patients with chronic inflammatory bowel disease.
Autoimmune cholangitis in the SJL/J mouse is antigen non-specific.
IgA antibodies to dietary antigens in liver cirrhosis.
Evolutionary distance from human homologs reflects allergenicity of animal food proteins.
Relationship between naturally occurring human antibodies to casein and autologous antiidiotypic antibodies: implications for the network theory.
Development of immune response to cow's milk proteins in infants receiving cow's milk or hydrolyzed formula.

'Roid Rage: Vitamin D3 - DO IT (Part I)

Naturally, we are all mildly worried about the swine flu (the delayed 'flu' season). Taking Vitamin D will certainly provide several layers of protection for our family and hopefully avert potential complications. Studies show 36% of individuals who are Vitamin D deficient develop respiratory infections (Reader's Digest).



What Vitamin D3 dose is considered appropriate?

Interestingly Cannell has not been too incorrect in his broad dosing dictum:
~1000 IU per 25-lb body weight


Dr. Cannell in fact is perfectly right on for dosing for 80% of the people that I have personally dosed for this steroid precursor to serum concentrations [25-OH-D] = 60-80 ng/ml.

Adults (Source: courtesy of Dr. Cannell's non-profit VitaminDCouncil.com)
Require 4000 to 10,000 IU daily (or even MORE) in the AM enough to provide serum blood levels of 25(OH)D 60-80 ng/ml.

Infants and Children

Infants and children under the age of one, should obtain a total of 1,000 IU (25 mcg) per day from their formula, sun exposure, or supplements. As most breast milk contains little or no vitamin D, breast-fed babies should take 1,000 IU per day as a supplement unless they are exposed to sunlight. The only exception to this are lactating mothers who either get enough sun exposure or take enough vitamin D (usually 4,000–6,000 IU per day) to produce breast milk that is rich in vitamin D. Formula fed babies should take an extra 600 IU per day until they are weaned and then take 1,000 IU a day, as advised below.

Children over the age of 1 year, and less than 4 years of age, should take 1,500 IU vitamin D per day, depending on body weight, latitude or residence, skin pigmentation, and sun exposure.

Children over the age of 4, and less than 10 years of age, should take 2,000 IU per day, unless they get significant sun exposure. On the days they are outside in the sun, they do not need to take any; in the winter they will need to take 2,000 IU every day.

Children over the age of 10 years old should follow instructions for adults detailed above.

My children get 20,000 IU on average PER WEEK and they're about 75lbs (but we have not been compliant patients and failed to get blood testing yet). We're lazy and they get 2 caps of the NOW Brand 5000 IU caps twice weekly, more or less. I require approx 5000 to 8000 IU daily (I'm about 128# right now *booh*) to keep my blood 70+ ng/ml and the Doctor and asthma inhalers away. Admittedly, as an adult, I rarely stay outdoors despite being a natural sun-worshipper. I get sick quite easily (like...if... anyone sneezes in my direction... b/c I not a carrior of warrior Lp(a)).

Thank Goodness for Dr. Davis (who's been raging about Vitamin D for 5 yrs)!

And the cholesterol-derived...Vitamin D!



They've saved my lungs (+tob cessation *!I know!!...quit 18mos ago*).

My kids as well!

For intermittent asthma, they were on/off inhalers and oral prednisone tapers which would routinely stunt their growth for a few months at a time. They are completely OFF everything...unless I go on vacation...when Daddy forgets. *aha*




Vitamin D and Athletic Performance

Dr. Cannell has written about the benefits of Vitamin D and athletic performance on his non-profit Vitamin D Council website as well as a recently summarized review article. Vitamin D is pro-hormone and a potent steroid. Don't underestimate it's powers. Vitamin D actually increases testosterone, estrogen, thyroid hormone and is a steroidal precursor to other sex and cholesterol hormone derivatives. It has actions in every organ, tissue and cell from the bottom of your hair follicles to the tip of your toe nails.

He has taken the time to review older German and Russian scientific literature on observations and studies on the influence of sun exposure/UV box exposure, seasonality effects on athletic performance.

Here are some of his thoughts from his website:

Improving Athletic Performance

"Then I remembered that several readers had written to ask me if vitamin D could possibly improve their athletic performance. They told me that after taking 2,000–5,000 IU/day for several months they seemed somewhat faster, a little stronger, with maybe better balance and timing. A pianist had written to tell me she even played a better piano, her fingers moved over the keys more effortlessly! Was vitamin D responsible for these subtle changes or was it a placebo effect? That is, did readers just think their athletic performance improved because they knew vitamin D was a steroid hormone precursor?

The active form of vitamin D is a steroid (actually a secosteroid) in the same way that testosterone is a steroid. It is also a hormone (hormone: Greek, meaning "to set in motion") in the same way that growth hormone is a hormone. Steroid hormones are substances made from cholesterol that circulate in the body and work at distant sites by setting in motion genetic protein transcription. That is, both vitamin D and testosterone set in motion your genome, the stuff of life. While testosterone is a sex steroid hormone, vitamin D is a pleomorphic steroid hormone.

All of a sudden, it didn't seem so silly. Certainly steroids can improve athletic performance—although they can be quite dangerous. In addition, few people are deficient in growth hormone or testosterone, so athletes who take sex steroids or growth hormone are cheating, or doping. The case with vitamin D is quite different because natural vitamin D levels are about 50 ng/mL and since almost no one has such levels, extra vitamin D is not doping, it's just good treatment. I decided to exhaustively research the medical literature on vitamin D and athletic performance. It took me over a year.

To my surprise, I discovered that there are five totally independent bodies of research that all converge on an inescapable conclusion: vitamin D will improve athletic performance in vitamin D deficient people (and that includes most people). Even more interesting is who published the most direct literature, and when. Are you old enough to remember when the Germans and Russians won every Olympics in the '60s and '70s? Well, it turns out that the most convincing evidence that vitamin D improves athletic performance was published in old German and Russian medical literature."

Is Vitamin D Supplementation PALEO?

Is... indoor-living... uhh... Paleo??


Um...hell-o . . . Supplementation provides what we cannot obtain in our daily living whether it is because we have to make a living INDOORS or we live above the 37th latitude in Northern Cal where UVB radiation is fairly negligible for nearly half the year. UVA (from tanning booths or sun, the wavelength which deeply penetrates glass and car windows and skin) does not unfortunately activate Vitamin D in the skin. My skin tone is dark in the summer therefore with sun exposure, for me, a high likelihood exists that the melanin pigmentation in fact blocks substantial UVB activation as a protective mechanism. It was not surprising to me in retrospective to find that the blood level was TOTALLY deficient at the end of Summer 2007 at 20 ng/ml, which was 400% away from the goal 80 ng/ml!


HOLY CR*P BATMAN.

No wonder I felt like S H * T.

For... 2+ decades of my LIFE.

The first winter...wow... I was on Vitamin D, I had the best running and half-marathons I've ever had (less struggling, less shortness of breath, less fatigue, better times) and... no asthma. Easy wt loss. (Did I say... EASY weight loss?) No breathing difficulties. No metered-dose-inhalers (MDIs). No coughing. Annually for the prior 3 yrs, I suffered from annual bronchitis where coughing fits sorta debilitated me for 6 to 8 wks at a time. (I thought it was from getting 'old'). Turned out the synthetic contraceptive I was on likely triggered the lack of protective natural estrogen, and blah blah blah. Anyhow, the vitamin D cured my (poss iatrogenic) bronchitis. No more antibiotic courses (which didn't work anyway). No more coughing spells (which tended to... frighten patients). No more sleeping problems. No more nasty codeine.


Is uninterrupted breathing important for athletic performance?

For living?

Are albuterol, salmeterol (Serevent, Advair) and other asthma beta-adrenergic agonist treatments banned by the IOC (Int'l Olympic Committee)?

Now you know why I roar and RAGE about the D's... Davis and the steroid 'D'.

Do the . . . right 'ROID. . . V I T A M I N - D3

Vitamin D: Nature's Antibiotic 20-50k IU daily x 3 days

FIG. 5. Antiinflammatory effects of vitamin D in the critically ill. Plasma concentrations of CRP and IL-6 serum concentrations over time in ICU are depicted for the two study groups. Open bars represent the low-dose 200 IU/d vitamin D group (n 10), and hatched bars represent the high-dose 500 IU/d group (n 12). Data are means SEM. Elevated CRP and IL-6 levels, observed on ICU admission, decreased significantly with time in ICU in both study groups. The fall in CRP was significantly more pronounced in the high-dose vitamin D group, compared with the low-dose group between d 3 and d 7; likewise in the high-dose group, IL-6 levels decreased from admission to d 4, whereas they remained unaltered in the low-dose group.
(*, P less than 0.05.)


I love vitamin D3 5000 IU from NOW brand in olive oil (iherb.com $8.80 per bottle of #120 capsules... at 12 bottles per case)...for optimal health and longevity *smile* and optimal flu/immunological protection)

ONE A DAY KEEPS THE PULMONOLOGIST AWAY...


And when I'm coming down with a cold . . . T-E-N (10) A DAY KEEPS THE FLU AWAY :)


In fact I've been using vitamin D as an antibiotic as well for the last 18 mos and have had very few colds. Prior to supplementation, I suffered from frequent URIs, coughing spells and bronchitis that would last 8wks or longer with little benefit from albuterol and steroid inhalers. (Lack of natural estrogen, suppressed by synthetic progestin, was the cause it turns out -- and yes the drug companies know this -- yes -- read the package insert of your contraceptive).

How do you know if you are vitamin D deficient? Frequent colds? Asthma? Hayfever/Allergies? Feel crappy, achy, sad sometimes? You probably have significant vitamin D deficiency. Most lab standard ranges post 'normal' vitamin D 25(OH)D as 30 to 100 ng/ml and this is clearly out dated and 'off.' Normal for outdoor living, non-makeup, non-sunscreen-wearing individuals is ~60-80 ng/ml, and this is what should be achieved via supplementation, sun and food (food is the poorest source unless you are Inuit on a high-fat-seal/seafood-diet). And...Forget about sunlight/UVB if you live away from the equator . . . y e s . . . that includes San Francisco and anything NORTH for about ~4-6 months per year.


Antibiotic dose ('Stoss' protocol): ~25,000 to 50,000 IU daily in the AM (or split) for 3 days

(Precise dose: 1000-2000 IU per kg (or 500 IU per ~pound))

Side Effects: wake up without sniffles, scratchy throat, green phlegm, chest tightness or asthma


The above study (graph) was a short one in a small number of critically ill patients. A 'high' dose vitamin D (only 500 IU/day) was more effective at lowering CRP, marker for inflammation, and IL-6, immune marker for infected-tissue destruction, compared with 'low' dose vitamin D (200 IU/day). What does this show? Not much except . . . (1) when one is critically ill the blood vitamin D concentration hit ROCK BOTTOM (why? it's nature's antiobiotic and restorative hormone) . . . and (2) even licking a vitamin D capsule will provide IMMENSE immunological benefit and may perhaps even save your life if you are ever critically ill.

As a kid one summer, I became almost critically ill after a mild-sized 3rd degree burn on my L-thigh (which I joking refer to as my 'shark bite' if people happen to ask). As a child, the area was a significant portion of body surface area and I was near comatose for a little while (my father doesn't even remember how long). Spending 24/7 outdoors in the hot humid Pennsylvania sun that summer prior to the accident probably provided some degree of vitamin D, I believe, to have afforded some protection, healing, and surviving (in addition to the antibiotics/steroids).
Bone turnover in prolonged critical illness: effect of vitamin D. PDF here. Van den Berghe G, Van Roosbroeck D, Vanhove P, Wouters PJ, De Pourcq L, Bouillon R. J Clin Endocrinol Metab. 2003 Oct;88(10):4623-32.



Below is info from Dr. Cannell and his non-profit Vitamin D Council on the curious antimicrobial protective effects and benefits of vitamin D.

May you and your family allude the flu this season!



http://www.vitamindcouncil.org/newsletter/2006-june-july.shtml

Is Vitamin D An Antibiotic?

Antimicrobial Peptides

"Dr. Liu and colleagues at UCLA, publishing in this March's edition of the prestigious journal Science, showed that vitamin D might be, in effect, a potent antibiotic. Vitamin D increases the body's production of naturally occurring antibiotics: antimicrobial peptides. Antimicrobial peptides are produced in numerous cells in the human body where they directly and rapidly destroy the cell walls of viruses and bacteria, including tuberculosis. Furthermore, Liu showed that adding vitamin D to African American serum (African Americans have higher rates of TB) dramatically increased production of these naturally occurring antibiotics.

Liu PT, Stenger S, Li H, Wenzel L, Tan BH, Krutzik SR, Ochoa MT, Schauber J, Wu K, Meinken C, Kamen DL, Wagner M, Bals R, Steinmeyer A, Zugel U, Gallo RL, Eisenberg D, Hewison M, Hollis BW, Adams JS, Bloom BR, Modlin RLToll-like receptor triggering of a vitamin D-mediated human antimicrobial response. Science. 2006 Mar
24;311(5768):1770–3.


Plenty of you have e-mailed me that pharmacological doses (high doses) of vitamin D (1,000–2,000 units/kg per day for three days), taken at the first sign of influenza, effectively reduces the severity of symptoms. However, has anyone ever studied giving 100,000, 200,000, or 300,000 units a day for several days to see if vitamin D induces antimicrobial peptides to help fight other life-threatening infections? (By the way, doses up to 600,000 units as a single dose are routinely used in Europe as "Stoss" therapy to prevent vitamin D deficiency and have repeatedly been shown to be safe for short-term administration.) No, you say, studies of "Stoss" therapy in serious infections have never been studied or reported in reputable journals. Well, maybe such treatment has been studied—and reported in the best journals—by way of the weirdest medical invention ever patented in the USA."