Monday, June 30, 2008

Lp(a): Running With Scissors (Part 1)

I'm sure as a kid, your mother warned you over and over and over how dangerous running with sharp objects is...

Or sharp pencils... Or knives... Or chopsticks...

Or Lp(a)??! wtf??

Ben Harper and friends: THERE WILL BE LIGHT
Rome Concert Live
Courtesy of

I wish we could live forever...

Then melt into the sun
Melt into the sun
Time is gonna change you
Once it gets you on the run
Gets you on the run


I've been running
Ever since
Ever since I was a child
Some call it free
And some call it wild

There will be
There will be
There will be a light
There will be a light
There will be
There will be
There will be a light
There will be a light

Why is Lp(a) elevated for some individuals? Why is it directly correlated with premature vascular disease (when BP is elevated)?

It's estimated there are potentially three families of factors that influence Lp(a) which affects about 17-25% of the general population:
(a) Structure and metabolism of very-low-density lipoprotein (VLDL) such as triglycerides, phospholipids, apoC-II, C-III, E, A-II and uric acid (which are of course ALL related to insulin)
(b) Thrombosis-related centering on platelets
(c) Acute phase reactions represented by 1 hr and 2 hr erythrocyte sedimentation rates (ESR) (in other words, immune system stimulation)
(I'd add a 4th factor in the formula (d) kidney dysregulation which is the site of Lp(a) catabolism and recycling/disposal in the human body)

Nakajima K, Hata Y. Intraindividual variations in lipoprotein (a) levels and factors related to these changes. J Atheroscler Thromb. 1996;2(2):96-106. PMID: 9225216

At we have several reports addressing Lp(a). The challenge in controlling this one single, severe plaque-building factor can not be underestimated. It can be an unrelenting foe...

-Lp(a) Report I (2006): Lipoprotein(a): What it is, why it's important, and why you need to know if you've got it!

-Lp(a) Report II (2008): Unique Strategies for Lipoprotein(a) Reduction

-Lp(a) Lipoprotein Checklist

There appear to be distinct subpopulations affected by Lp(a) from my (anecdotal, untrained) nonscientific observations:

--high-carb consuming well known athletes (and unknown) who drop dead at endurance events of MIs (Brian Maxwell Northern Cal POWERBAR guru, Jim Fixx, and lucky survivor-Alberto Salazar)
--advanced stage chronic kidney disease (CKD)
--end-stage-renal-disease (ESRD) and dialysis patients
--individuals with kidney stones
--individuals with Metabolic Syndrome (MetSyn) with premature heart disease in the family tree (females affected before age 65; males affected before age 55)
--men with diabetes Type 2 and erectile dysfunction
--individuals with MetSyn who have survived cancer (a condition that really sets off acute phase reactions and the immune system to heal)
--youth and young children with MetSyn, esp PCOS or any other hormone derangements (ie, wheat addiction/prolactin, big-man-boobs, appear 4-mos pregnant and they are male )
--children with elevated insulin and apo B
--adults with elevated insulin and apo B (and this is much more toxic for women for some reason than men)
--women after menopause, esp if no hormone replacement occurs

Can we avoid the dangers of running with scissors (or chopsticks)?

I certainly believe so. (Heed the words of your mother)

Let's keep running... wild and free... until we melt with the sun...

Lp(a): PPAR-Delta... Dagger in the Heart of Lp(a) (Part II) coming soon...

Monday, June 23, 2008

Control Insulin (Part Two)

Briefly, the history of insulin and its relationship to atherosclerosis:

Stout RW. Insulin and atheroma. 20-yr perspective. Diabetes Care. 1990 Jun;13(6):631-54. Review. PMID: 2192848 Department of Geriatric Medicine, Queen's University of Belfast, Northern Ireland.
Many clinical studies have shown an increased insulin response to oral glucose in patients with ischemia of the heart, lower limbs, or brain. Hyperinsulinemia also occurs in patients with angiographically proved atherosclerosis without ischemia and thus appears to be related to arterial disease and not to be a nonspecific response to tissue injury. Fasting insulin levels and insulin responses to intravenous stimuli, including glucose, tolbutamide, and arginine, are normal, suggesting a gastrointestinal factor may be involved in the increased insulin response to oral glucose. In patients with atherosclerosis, insulin sensitivity appears to be normal or enhanced with respect to both glucose and lipid metabolism. Five population studies have shown that insulin responses to glucose are higher in populations at greater risk of cardiovascular disease. Many of the hyperinsulinemic populations also had upper-body obesity, hypertriglyceridemia, lower high-density lipoprotein (HDL) levels, and hypertension. These prospective studies support an independent association between hyperinsulinemia and ischemic heart disease, although their results differ in detail. Hyperinsulinemia is associated with raised triglyceride and decreased HDL cholesterol levels. Total and low-density lipoprotein (LDL) cholesterol is less closely related to hyperinsulinemia. Upper-body adiposity is associated (in separate studies) with coronary heart disease, diabetes, hyperinsulinemia, and hypertriglyceridemia. Insulin and blood pressure are closely related in both normotensive and hypertensive people. Although obesity and diabetes are often found in hypertensive people, hyperinsulinemia also occurs in nonobese nondiabetic hypertensive people. Thus, hyperinsulinemia is closely associated with a cluster of cardiovascular risk factors, i.e., hypertriglyceridemia, low HDL levels, hypertension, hyperglycemia, and upper-body obesity. There is a possibility that insulin has a role in the sex differences in ischemic heart disease incidence and their absence in diabetes, but additional work is required for its clarification. Long-term treatment with insulin results in lipid-containing lesions and thickening of the arterial wall in experimental animals. Insulin also inhibits regression of diet-induced experimental atherosclerosis, and insulin deficiency inhibits the development of arterial lesions. Insulin stimulates lipid synthesis in arterial tissue; the effect of insulin is influenced by hemodynamic factors and may be localized to certain parts of the artery. In physiological concentrations, insulin stimulates proliferation and migration of cultured arterial smooth muscle cells but has no effort on endothelial cells cultured from large vessels. Insulin also stimulates cholesterol synthesis and LDL binding in both arterial smooth muscle cells and monocyte macrophages.

Despres JP et al showed in the below study how elevated fasting insulin blood levels was closely associated to the presence of ischemic heart disease. The higher the concentration of insulin, the greater the odds ratio. And additionally they found other factors compounded the risk of heart disease:
--High Triglyercides
--High Total/HDL ratio (in other words, low HDL)
--High Apolipoprotein B

Després JP, Lamarche B, Mauriège P, Cantin B, Dagenais GR, Moorjani S, Lupien PJ.Hyperinsulinemia as an independent risk factor for ischemic heart disease.N Engl J Med. 1996 Apr 11;334(15):952-7. PMID: 8596596

Figure. Odds Ratios for Ischemic Heart Disease according to Plasma Insulin and Triglyeride Concentrations, Total:HDL Cholesterol Ratios, and Apolipoprotein B Concentrations. Insulin was measured after subjects had fasted for 12 hours. The median TG concentration (150 mg/dl [1.7mmol/L]), total:HDL ratio (6.0), and apoplipoprotein B concentration (119 mg/dl) were used to define men with either low levels (below the 50th percentile) or high levels (at or above the 50th percentile) for these variables. The results of tests of multiplicative interactions did not reach signficance at the 0.05 level for any of the combinations. P values are for comparisons with the reference group, which was assigned an addos ratio of 1.0. To convert values for insulin to picomoles per liter, multiply by 6.

The researchers Lemarche et al have done a great deal of research examining 'non-traditional risk factors '(see Table 2) and also showed the same link between insulin and associated ischemic heart disease.
Lamarche B, Tchernof A, Mauriège P, Cantin B, Dagenais GR, Lupien PJ, Després JP. Fasting insulin and apolipoprotein B levels and low-density lipoprotein particle size as risk factors for ischemic heart disease. JAMA. 1998 Jun 24;279(24):1955-61. (Full PDF here) PMID: 9643858

In fact, their results uncovered the fact that the largest odds ratio between traditional (LDL, TG, HDL) and nontraditional (small dense LDL, apo B and fasting insulin) fell to the Hyperinsulinemia risk factor. So high fasting insulin correlated stronger with the presence of evidence of coronary artery disease than than LDL-cholesterol. Triglyericides (TGs) even associated to a higher degree than LDL-cholesterol. HHmmmm?

Why do we always call LDL the 'bad' cholesterol? It appears that TGs is a bad character, indeed it appears TGs are the worse cholesterol out of all the traditional risk factors! Dr. Davis has pursued a lower TG goal lower than 'traditional' guidelines for many years. Current 'conventional' cardiovascular advice aims for TGs less than 150 however the Track Your Plaque program advocates an aggressive TG goal of 'normal' less than 60.

Is the 'LDL-cholesterol hypothesis' completely bunk?

Shouldn't Triglyerides be known as the 'lousy/bad' cholesterol?

Is this why statin-monotherapy fail to prevent signficant mortality and morbidity caused by plaque in heart disease and strokes?

The TYP goals for regression of ischemic heart disease are 60-60-60-60 (TG-HDL-LDL-25(OH)D). Many achieve this and beyond -- HDLs 80-90s and TGs 25-50s in the program!

And Elevated Fasting Insulin goal is not just less than 12 mU/L as discussed in the 2nd study above but at TYP the goal for regression is normal fasting insulin levels less than 5-10 mU/mL (30-60 pmol/L).

Is this why the Track Your Plaque program controls plaque comprehensively and trumps all 'conventional' cardiology programs by controlling triglycerides and insulin by a multifaceted strategy?
--Vitamin D3
--Wheat and grain cessation
--Weight loss to achieve normal BMI
--High/ultra-high dose fish oil EPA+DHA
--Hormone optimization (estrogen, testosterone, DHEA, etc)
--Vitamins K2/E/A
--Et cetera

Conclusions by the above authors Lamarche, et al:
'Beyond the mechanisms underlying the atherogenicity of hyperinsulinemia, hyperapobetalipoproteinemia, and small, dense LDL, and irrespective of whether these mechanisms share common paths, results of the present study suggest that the risk of IHD is increased substantially when these metabolic abnormalities cluster. The synergistic contribution of the nontraditional cluster of risk factors to IHD risk and the fact that almost 1 of every 2 IHD cases had these abnormalities simultaneously reflect the multifactorial etiology of IHD. It also emphasizes the importance of defining the risk of IHD based on more than 1 risk factor.
There are a number of critical issues that have to be considered before any decision can be made toward the measurement of these nontraditional risk factors on a routine basis. Among others, results of this prospective case-control study will have to be confirmed through larger population-based studies, as the relatively low number of IHD cases allowed only a gross assessment of risk. The relatively large CIs associated with the estimated risk in some of the subgroups reflect this phenomenon. Population reference values such as those used for LDL-C, triglycerides, and HDL-C also will be needed before critical levels of fasting insulin, apolipoprotein B levels, and LDL particle size or density at which a person becomes at greater risk for IHD are identified. Means to achieve effective treatment of the nontraditional risk factors is also a critical issue that deserves a great deal of scrutiny before decisions can be made toward use of these variables in the risk management of IHD. There are data to suggest that LDL particle size can be modulated by changes in plasma triglyceride levels.
41 Studies have shown that triglyceride-lowering therapy with fibric acid derivatives can lead to a significant increase in LDL particle size.42-43 There is also a large body of evidence demonstrating that LDL particle size, apolipoprotein B level, and insulin resistance and/or hyperinsulinemia can be effectively altered by diet and exercise-induced weight loss.44-45 Thus, the ability to favorably modify the nontraditional risk factors by diet, exercise, and appropriate pharmacotherapy provides further support for the use of these risk factors in the management of IHD risk...'

Lawlor DA, Fraser A, Ebrahim S, Smith GD. Independent associations of fasting insulin, glucose, and glycated haemoglobin with stroke and coronary heart disease in older women. PLoS Med. 2007 Aug;4(8):e263. PMID: 17760500
Full PDF here:

Editor's Summary
Background: Narrowing of the vessels that take blood to the heart and brain is a common form of cardiovascular disease—i.e., a disorder of the heart and blood vessels. It is a major cause of illness and death. By starving the heart and brain of oxygen, this condition causes coronary heart disease (CHD; heart problems such as angina and heart attacks) and strokes. A major risk factor for CHD and strokes is diabetes, a common chronic disease characterized by high levels of sugar (glucose) in the blood. In people who don't have diabetes, the hormone insulin controls blood-sugar levels. Insulin, which is released by the pancreas after eating, “instructs” insulin-responsive muscle and fat cells to absorb the glucose (released from food) from the bloodstream. In the very early stages of type 2 diabetes (the commonest type of diabetes, also called “adult onset” or “noninsulin-dependent” diabetes”), muscle and fat cells become unresponsive to insulin, so blood-sugar levels increase. This is called “insulin resistance.” The pancreas responds by making more insulin. As a result, people with insulin resistance have high blood levels of both insulin (hyperinsulinemia) and glucose (hyperglycemia). Eventually, the insulin-producing cells in the pancreas start to malfunction, insulin secretion decreases, and type 2 diabetes is the result.
'Our findings indicate that amongst older women without diabetes and with fasting glucose levels in the normal range, fasting insulin is a stronger predictor of CHD and stroke risk than are fasting glucose or HbA1c.'
In addition, the results demonstrated a 'positive linear association between fasting insulin and CHD and stroke events is consistent with findings from the Atherosclerosis Risk in Communities study (SEE LAST CITATION), in which there was a positive linear association with CHD events that remained after adjustment for other CHD risk factors amongst women, but not amongst men [27]. A metaregression analysis of 17 prospective studies, primarily conducted in men and younger age groups than the current study, found a pooled relative risk of CHD per 50 pmol/l of insulin of 1.18 (95% CI 1.08–1.29) [9], which is consistent with our fully adjusted association with CHD (our results equate to 1.13 [95% CI 1.01–1.27] per 50 pmol/l of insulin). Overall the evidence suggests a modest positive association between fasting insulin and CHD events in women and men. Fasting insulin may exert its effect on cardiovascular risk via a direct impact on endothelial function [28,29].'

CRACK DOWN on insulin... CRACK DOWN on plaque (and cancer)...

Hunger will disappear away as well. Part of insulin's purpose is to drive energy into cells for storage. Insulin drives hunger as well. (...and mainly the consumption of carbs drive insulin secretion)
You will realize the benefits of low blood insulin and will often 'forget' to eat without prompting from this powerful hormone. You'll hunger for other things... vitality, movement, effortless-boundless ENERGY.

Importance of controlling triglycerides and insulin:


Zavaroni I, Dall'Aglio E, Alpi O, Bruschi F, Bonora E, Pezzarossa A, Butturini U.
Evidence for an independent relationship between plasma insulin and concentration of high density lipoprotein cholesterol and triglyceride.
Atherosclerosis. 1985 Jun;55(3):259-66.
PMID: 3893447 [PubMed - indexed for MEDLINE]

Ghiselli G, Bon GB, Soldan S, Avogaro P.
Regulatory function of glucose and insulin on high-density lipoprotein cholesterol in normolipidemic subjects.
Metabolism. 1994 Nov;43(11):1332-7.
PMID: 7968586 [PubMed - indexed for MEDLINE]

Cominacini L, Garbin U, Davoli A, Campagnola M, De Santis A, Pasini C, Pastorino AM, Bosello O.
High-density lipoprotein cholesterol concentrations and postheparin hepatic and lipoprotein lipases in obesity: relationships with plasma insulin levels.
Ann Nutr Metab. 1993;37(4):175-84.
PMID: 8215234 [PubMed - indexed for MEDLINE]

Laws A, King AC, Haskell WL, Reaven GM.
Relation of fasting plasma insulin concentration to high density lipoprotein cholesterol and triglyceride concentrations in men.
Arterioscler Thromb. 1991 Nov-Dec;11(6):1636-42.
PMID: 1931867 [PubMed - indexed for MEDLINE]

Stalder M, Pometta D, Suenram A.
Relationship between plasma insulin levels and high density lipoprotein cholesterol levels in healthy men.
Diabetologia. 1981 Dec;21(6):544-8.
PMID: 7040144 [PubMed - indexed for MEDLINE]

Tchernof A, Lamarche B, Prud'Homme D, Nadeau A, Moorjani S, Labrie F, Lupien PJ, Després JP.
The dense LDL phenotype. Association with plasma lipoprotein levels, visceral obesity, and hyperinsulinemia in men.
Diabetes Care. 1996 Jun;19(6):629-37.
PMID: 8725863 [PubMed - indexed for MEDLINE]

Laws A, Reaven GM.
Evidence for an independent relationship between insulin resistance and fasting plasma HDL-cholesterol, triglyceride and insulin concentrations.
J Intern Med. 1992 Jan;231(1):25-30.
PMID: 1732395

Katzel LI, Coon PJ, Rogus E, Krauss RM, Goldberg AP.
Persistence of low HDL-C levels after weight reduction in older men with small LDL particles.
Arterioscler Thromb Vasc Biol. 1995 Mar;15(3):299-305.
PMID: 7749838

McNamara JR, Jenner JL, Li Z, Wilson PW, Schaefer EJ. ***
Change in LDL particle size is associated with change in plasma triglyceride concentration.
Arterioscler Thromb. 1992 Nov;12(11):1284-90.
PMID: 1420088

Folsom AR, Szklo M, Stevens J, Liao F, Smith R, Eckfeldt JH. **
A prospective study of coronary heart disease in relation to fasting insulin, glucose, and diabetes. The Atherosclerosis Risk in Communities (ARIC) Study.
Diabetes Care. 1997 Jun;20(6):935-42.
PMID: 9167103


Sunday, June 22, 2008

Control Insulin, Control Plaque... (And Cancer)

Killa Whale
By Nickatina
Advisory: lyrics NSFW
(For sensitive ears... resist... the urge... to c-l-i-c-k)
'Track, Smack, Whack Plaque' as HH
always says... extinguish plaque for an eternity.
Forge elite heart fitness...
BTW this song rocks when thrashin' at Crossfit...

Chewy boy, doobie with the buddha cess...
So read my mind, the situation's critical...
You think you know me?
Well test your luck and try me out...

Then watch that valium on your dome
I'm putting beary fairy nig*** in a state of shock (shock!)
And I'm a killa whale but nigga check my pit lock
So bust that, crush that, crush that
Cuh-crack crack!

...I'm harmon like that wolverine
Deadly like that Octagon
Fillmoe to the fu*** heart
Crooked like the Pentagon

...So check my rep, survival tech, and hit man killa tactics
Nig*** get berry faced down on silver plastic...
The fat rat dominator, microphone terminator
Quick to break the neck of an E-40 imitator

Nig*** don't front, you know I got you open
With more Raider in me than they ever had in Oakland
To all you moth*** that juss can't tell
I'm a Pisces but I'd rather be a KILLA WHALE

Controlling insulin reaps many rewards. As the previous article suggests, insulin is an ancient hormone ubiquitous in all animals -- from worms to humans -- with classic/nonclassic responsibilities including (see Table 1). Some of these actions are beneficial like Thermogenesis, however many of the others are detrimental in the great majority of situations:
--low potassium
--raised heart rate
--increased uric acid (ie, gout)
--increased clotting
--CNS stimulation (ie, anxiety, epression, ADHD)
--prevention of fat from being liberalized for energetic uses

We require only tiny, neglible amounts of insulin for thermogenesis and shuttling of energy (glucose) into muscles and liver for storage.

In fact, increased energy expenditure is exponentially increased when insulin resistance is kept at bay. What is insulin resistance (IR)? It is like being at a rock concert (or Hannah Montana venue with screaming little girls everywhere) where temporary hearing loss is induced by inclement noise pollution. As soon as the volume returns to a low level, hearing resumes. Shut insulin down by going grain-free, carb-restricted, intermittent fasting and exercising, then inflammatory responses and processes are cut off. The same research demonstrated that men and women have blunted energy expenditure when the 'volume of insulin' is dialed exceptionally high. And for us women, we may even have a 'negative' energy output (in other words 'storage') with energy expenditure during the presence of insulin resistance... huhhh??! Talk about an exceedingly 'thrifty' gene... *urgh* Insulin-resistant gals gain weight with exercise... how exceedingly unfair. This actually is a common phenomenon and very discouraging for women trying to lose weight and fight an uphill battle as they eat per conventional medical advice 'low fat'/high-carbohydrate/insulin-inducing diets (USDA 'whole grain' pyramidal nonsense).

Degrees of IR can also be effectively cranked down by (Isharwal S, et al. Dietary nutrients and insulin resistance in urban Asian Indian adolescents and young adults.Ann Nutr Metab. 2008;52(2):145-51.):
--normal BMI achievement
--reduction of pro-inflammatory omega-6 oils
--increase of anti-inflammatory omega-3 EPA+DHA oils (ie, cod liver, fish oil, pasture-fed milk, meat, eggs, etc)

And of course...wheat avoidance, grain elimination, carb restriction, intermittent fasting and exercise.

Excessive insulin (ie, hyperinsulinemia) leads to the below changes (see below diagram):
--generation of TGs and small dense atherogenic LDL
--conversion from fatty streaks to plaque
--plaque growth
--increased adipose tissue mass (Obesity, Metablic Syndrome, PCOS)
--accumulation of Triglycerides in non-adipocytes
--nonalcoholic steatohepatitis (fatty liver/NAFLD)
--pancreatic beta-cell failure (fatty pancreas, insulin resistance)
--dilated cardiomyopathy (myocyte (heart cell) stiffening and diastolic dysfunction)
--arterial stiffening
--blood glucose spikes
--expansion of visceral fat (belly fat colonies)
--fatty liver, fatty pancreas, fatty gallbladder, fatty heart
--Diabetes Type 2
--strokes, heart attacks
--cancer (see end)

So... when insulin becomes rampant and uncontrolled like ex-KGB-satellites gaining prominence and power to control global McMafia-like franchises for cocaine, opioid, and crack trafficking, then world and global economies are undoubtedly affected. Whole human systemic organ functions become dominated by hyperinsulinemia, leading to all sorts of dysfunction and energy dysregulation. Why rely on primitive petrol... when nuclear power exists?

Fig 1. Lipotoxicity in humans originates from excessive release of free fatty acids from hypertrophied adipocytes in obese persons. Organ exposure to high levels of free fatty acids causes lipid droplets to accumulate within the cytosol of nonadipose tissues in proximity to mitochondria (white arrows, bottom).By-products of cytosolic triglyceride accumulation and of lipid metabolism may lead to organ dysfunction and failure. McGavock JM, Victor RG, Unger RH, Szczepaniak LS. Adiposity of the heart, revisited. (Full PDF here.) Ann Intern Med. 2006 Apr 4;144(7):517-24. Review. PMID: 16585666

The inflammation associated with insulin is akin to the oxidative damage that occurs when soft materials like rubber or plastic is left outside exposed to the elements. Over time, the rubber hardens and becomes inelastic and rigid, easily breaking with any shear force. Sort of like running a high-powered hose made out of glass, right? With the elimination of inflammatory influences, human tissues can return to their original soft, elastic, pliable states. This includes endothelium, heart blood vessels, contractile tissues like our heart and skeletal muscles... even our oral gum tissues!

Reversal occurs when insulin is shut down.

The previous review of the research eloquently illustrates the special properties that dictate this ancient 'reactive' hormone. Insulin is one of the few hormones that is controlled by consumed 'substrates'.... What is in charge of turning insulin on and off? What are substrates of insulin?


Found in our daily meals and snacks! What we consume indeed dictates what we are (biochemically speaking).

Food composition directly lowers or raises insulin concentrations. Various other factors of course determine how quick and how sustained hyperinsulinemia occurs (exercise, weight loss, skeletal muscle dominance, size and location of visceral fat colonies (ie, 'belly' is 'bad') but in essence our food controls blood insulin levels.

If what we put in our mouth dictates are insulin levels, then equally powerful is what we don't... In other words, processes like starvation, skipping meals, random eating, intermittent fasting and going low-carb or restricted-carb are ways to reduce and control insulin. Consumption of adequate protein and fats and fiber control insulin release as well.

Take powerful control over plaque and inflammatory processes by shutting insulin secretion off. At Track Your Plaque the Paleo grain-free diet produces the best plaque-busting results. Consider the complete avoidance of all wheat and grains:
--wheat products (incl cereal, pasta, noodles, bread, crackers, pita, tortilla)
--bulgur (cracked wheat)
--oat (except oat bran)
--corn (incl popcorn, grits, cornmeal, tortilla, chips)
--et cetera

Consume most of the carbohydrates from non-starchy vegetables and raw nuts/seeds and low-GI fruit like berries.

Controlling insulin not only controls CAD but also controls cancer... Is 'whole grains' just promoting 'whole C-A-N-C-E-R'? As well as 'whole CORONARY ARTERY DISEASE'?
--breast cancer
--prostate cancer
--colon cancer
--pancreatic cancer

  • Berstein LM. Endocrinology of the wild and mutant BRCA1 gene and types of hormonal carcinogenesis. Future Oncol. 2008 Feb;4(1):23-39. Review. PMID: 18240998
  • Hede K.Doctors seek to prevent breast cancer recurrence by lowering insulin levels.
    J Natl Cancer Inst. 2008 Apr 16;100(8):530-2. PMID: 18398091
  • Barnard RJ.Prostate cancer prevention by nutritional means to alleviate metabolic syndrome. Am J Clin Nutr. 2007 Sep;86(3):s889-93. Review.PMID: 18265484
  • Park JH.Inhibition of colon cancer cell growth by dietary components: role of the insulin-like growth factor (IGF) system. Asia Pac J Clin Nutr. 2008;17 Suppl 1:257-60. PMID: 18296350
  • Tenenbaum A, et al. Does the lipid-lowering peroxisome proliferator-activated receptors ligand bezafibrate prevent colon cancer in patients with coronary artery disease? Cardiovasc Diabetol. 2008 Jun 19;7(1):18. PMID: 18565233
  • Pisani P. Arch Physiol Biochem. 2008 Feb;114(1):63-70. Hyper-insulinaemia and cancer, meta-analyses of epidemiological studies.

    Background: A substantial body of evidence links sex hormones, diet, excess body weight and physical activity to the risk of developing cancer at several sites common in affluent countries. The hypothesis that high circulating levels of insulin could be the underlying factor increasing cancer risk has been proposed. Epidemiological studies on markers of hyper-insulinaemia and cancer are reviewed and summarized. Methods: Studies of cancers of the colon and rectum, pancreas, breast, and endometrium examining the association with blood levels of C-peptide, insulin, glucose, glycated haemoblobin (HbA1c) were searched in PubMed. Multivariate, adjusted relative risks (RR) and their 95% confidence intervals were abstracted and summarized by meta-analyses. Results: Most of the studies identified were cohorts that relied on measurements obtained at baseline or assessed in blood stored at low temperature several years before the onset of cancer. The meta-analyses showed excess risks of colorectal and pancreatic cancers associated with higher levels of circulating C-peptide/insulin and with markers of glycaemia. Significant heterogeneity was found among four epidemiological studies of endometrial cancer and C-peptide giving a summary RR compatible with no association. Overall breast cancer risk was significantly higher in the upper categories of C-peptide/insulin, however, the excess derived entirely from retrospective studies. Conclusion: Current evidence suggests that subjects who develop colorectal and pancreatic cancers have increased pre-diagnostic blood levels of insulin and glucose. PMID: 18465360

Sunday, June 15, 2008

'Wanted': Elite Heart Health NOW

There is a new summer blockbuster I'm looking forward to...(!!) 'Wanted' shortly will be released. Angelina Jolie plays a sort of 'trainer'... to a novice apprentice. All the tools to assassinate the target are provided, and he is 'invited' to lead a new life. Do we all have opportunities to transcend and create extraordinary goals? ...And achieve what we never dreamed? Would you know unless the first steps are taken? Do you need a trainer?

Shift time... Shift your destiny... and make every minute count.

Live like you mean it

Don't accept a 'normal' standard heart life (ie, 'conventional cardiovascular care')
Don't expect mediocrity
Don't wait for an AED defibrillator to be mandated for each home for a home myocardial infarction
Don't play with fire...

Protect a life, yours, and protect others, those who depend on you

Learn all the weapons to l-i-v-e... super-vital, plaque-free, extra-extended lives

Forge elite heart health and fitness now

'This is your destiny. Join us...' Morgan Freeman

Choose your destiny

Choose elite heart health now...And change your life forever...

Track Your Plaque (TYP 2.0):
--controls plaque
--controls weight and body fat
--controls TGs ('bad cholesterol') and small dense bullet-like LDL
--controls blood pressure
--controls inflammation and insulin
--controls glucoses
--controls heart rhythms
(These interventions also controls the same factors which cause strokes, ED, and most cancers.)

Do you need a trainer?


Friday, June 13, 2008

Ancient Insulin... Modern Metabolic Chaos and Cancer

When the Russian empire fell, civil, political, financial chaos ensued. A new book titled McMafia recently came out. The author Misha Glenny recently appeared on Charlie Rose to discuss what his investigative reporting illuminated over the last few years. He made interesting comments about how the ex-KGB were suddenly in essence 'forced' to command new 'mafia-like' outposts after the regime was re-ordered (or dysregulated). Naturally, the public could not rely on the state for policing. Who was more sophisticated and trained? Real mafia or the government-sponsored with access to the latest research, gadgets, military surveillance and satellite technology? Actually, that may be a difficult one to answer... Naturally, a new order was created and in fact so well the author reports that they now run dominant global operations (demonstrating strong entrepreneurial spirit! and franchise facets!).

Similar derangement (and 'reconfiguration' of diseased organs) occurs when carbohydrates are introduced to human metabolism...Chaos, inflammation, blood thickening, increased heart rate, lower TSH, higher cortisol (more neuropsych issues; sodium retained), high uric acid (UA;gout), high blood pressure, decreased vagal tone (more anxiety), vascular tone goes down the drain (leading to plaque an arterial stiffness). Cancer...? Coronary artery disease...? Even mental derangement (like PMS, ADHD, depression)?

Kinda like putting water in your gas tank... Need a little humidity and moisture for petrol/gasoline to flow, however if excessive water mixes in, the engine and carburetor will eventually be ruined.

Approximately ten years ago, Ferrannini et al wrote a revised canon for insulin actions entitled 'Insulin: New Roles for an Ancient Hormone.' Insulin not only has several responsibilities including the process of transporting energy (glucose) into muscles and the liver, but also has many other actions when excessive and over-represented and un-directed. Insulin is an ancient peptide hormone and evolutionarily tightly conserved -- expressed in tissues of all species vertebrate and non-vertebrate... including C.elegans the longevity worm-model. What is the downstream effect of insulin on worms? Shortened lifespan.

The funny thing about this peptide hormone is that there is no direct central controller. It is like a de-centralized satellite KGB agent. No pituitary or hypothalamic hormone flips insulin 'on' or 'off'. The authors wrote insulin's 'release is driven by its substrate, with no apparent central integration.'

Insulin: new roles for an ancient hormone.
Ferrannini E, et al. Eur J Clin Invest. 1999 Oct;29(10):842-52.

Recent research has greatly expanded the domain of insulin action. The classical action of insulin is the control of glucose metabolism through the dual feedback loop linking plasma insulin with plasma glucose concentrations. This canon has been revised to incorporate the impact of insulin resistance or insulin deficiency, both of which alter glucose homeostasis through maladaptive responses (namely, chronic hyperinsulinaemia and glucose toxicity). A large body of knowledge is available on the physiology, cellular biology and molecular genetics of insulin action on glucose production and uptake. More recently, a number of newer actions of insulin have been delineated from in vitro and in vivo studies. In sensitive individuals, insulin inhibits lipolysis and platelet aggregation. In the presence of insulin resistance, dyslipidaemia (HIGH TGs, LOW HDLs, HIGH apoB, HIGH Lp(a)), hyper-aggregation and anti-fibrinolysis may create a pro-thrombotic milieu. Preliminary evidence indicates that hyperinsulinaemia per se may be pro-oxidant both in vitro and in vivo. Insulin plays a role in mediating diet-induced thermogenesis, and insulin resistance may therefore be implicated in the defective thermogenesis of diabetes. In the kidney, insulin spares sodium and uric acid from excretion; in chronic hyperinsulinaemic states, these effects may contribute to high blood pressure and hyperuricaemia. Insulin hyperpolarises the plasma membranes of both excitable and non-excitable tissues, with consequences ranging from baroreceptor desensitisation to cardiac refractoriness (prolongation of QT interval). Under some circumstances insulin is vasodilatory-the mechanism involving both the sodium-potassium pump and intracellular calcium transients. Finally, by crossing the blood-brain barrier insulin exerts a host a central effects (sympatho-excitation, vagal withdrawal, stimulation of corticotropin releasing factor), collectively resembling a stress reaction. Description and understanding of these new roles, their interactions, the interplay between insulin resistance and hyperinsulinaemia, and their implications for cardiovascular disease have only begun. PMID: 10583426

The insulin receptor: a new ANTI-CANCER target for peroxisome proliferator-activated receptor-gamma (PPARgamma) and thiazolidinedione-PPARgamma agonists.

Costa V, et al. Endocr Relat Cancer. 2008 Mar;15(1):325-35.

The peroxisome proliferator-activated receptor-gamma (PPARgamma) is a member of the nuclear hormone receptor superfamily. Ligand activation of PPARgamma is associated with differentiation and inhibition of proliferation in the normal and malignant cells. Herein, we studied the effects of PPARgamma and the PPARgamma agonists thiazolidinediones (TZDs) on the insulin receptor (IR), a cell membrane tyrosine kinase receptor protein, whose role is of paramount importance in mediating the metabolic and growth-promoting effects of the peptide hormone insulin. Overexpression of the PPARgamma1 in human hepatocellular (HepG2) cells was associated with decreased IR gene transcription and protein expression levels, and these reductions were more evident in the presence of TZDs. Since no PPARgamma response elements were identified on the IR promoter, we postulated that PPARgamma adversely affects the IR gene transcription by perturbing the assembly and stability of the transcriptionally active multiprotein-DNA complex identified previously, which includes the high-mobility group A1 protein, the ubiquitously expressed transcription factor (Sp1), the CAAT enhancer-binding protein (C/EBPbeta), and, in some cell lines, the developmentally regulated activator protein-2 (AP-2) transcription factor. Using glutathione S-transferase pull-down assays combined with electrophoretic mobility shift assay and chromatin immunoprecipitation, we demonstrated that by interacting with Sp1, C/EBPbeta, and AP-2, PPARgamma can prevent Sp1/AP-2 protein-protein association and inhibit binding of Sp1 and C/EBPbeta to DNA, thus reducing IR gene transcription. Our results demonstrate that IR is a new target gene of PPARgamma, and support a potential use of TZDs as anti-proliferative agents in selected neoplastic tissues overexpressing IRs. PMID: 18310298

Saturday, June 7, 2008

Wheat: Raises Insulin and Upregulates 'Bad' Genes

Ancient Wheat: 'Gladiator '
'Now We Are Free' Hans Zimmer, Lisa Gerrard

Can our food alter gene expression?

Absolutely so!

As Hippocrates once said, 'Let food by thy Medicine... and Medicine thy Food.' I'm sure he didn't mean medications as they exist now as chemicals or benzene rings (derived from petroleum) mass synthesized in factories for global consumption. The below FUNGENUT study recently showed the importance of how different sources of carbohydrate containing foods immediately changes gene expression in our favorite organ -- the omentum -- the stubborn fat lying on our bellies -- yes, the one covering up your those fabulous 6-pack abs. (Diagram: Ludwig, D. (2002) JAMA )

In a small group of subjects, 2 diets (Rye-Pasta -- mildly lower in GI; Oat-Wheat-Potato -- high GI carbs) were compared for 3 months. At the end no change in weight or insulin resistance, insulin levels, or glucose concentrations occurred. The profile for insulin (1st phase) secretion mildly improved in the Rye-Pasta group.
Interestingly, other than showing that wheat sucks (and perhaps oat and potato) gene expression was entirely affected by simple changes in carbohydrate content and the Glycemic Index (GI measures how long and how fast glucose enters the blood stream after consumption). Rye (endosperm) bread has a GI (glycemic index) of approximately 60-70. Pasta's GI is about 60-70 as well (depending on the type and how al dente/not-overcooked).

Wheat bread on the other hand is about 90-100 (close to pure glucose). Oats about 70 and potatoes 80-100 (without cream or butter which slows the uptake of starches into the stomach blood circulation which would effectively lower the GI). American Russet potato even exceeds glucose, 110 (!wow).

"Prior microarray studies found differences in gene expression between overweight and lean individuals (2) and after energy restriction (3); however, changes in the ratio of fat to carbohydrate did not alter gene expression (3). The study by Kallio et al makes a significant contribution to the literature by demonstrating the potentially major effects of dietary composition on gene regulation, independent of energy intake and body weight. Two specific findings concerning the low-insulin-response diet merit particular attention: the down-regulation of both hormone-sensitive lipase (HSL) and TCF7L2. "

"HSL, a key enzyme in the release of fatty acids from adipose tissue, has been proposed to affect body weight and metabolic variables. Mice made deficient in HSL by genetic manipulation are resistant to genetic- or diet-induced obesity (4, 5). Women carrying an allele associated with decreased HSL activity have lower fasting and simulated insulin concentrations, and men with this allele have lower nonesterified fatty acid concentrations (6)..."

"The transcription factor TCF7L2 is the strongest known genetic predictor of type 2 diabetes. A microsatellite within intron 3 of this transcription factor occurs with increased frequency in individuals with type 2 diabetes, which corresponds to an estimated population attributable risk of 21% (7)..."

"The present study (BELOW) has direct implications concerning our understanding of the dietary glycemic index (GI). The GI is a system for classifying carbohydrate-containing foods according to how blood glucose concentrations change in the postprandial period (reviewed in reference 8). High-GI meals produce greater postprandial insulin concentrations and C-peptide excretion than do nutrient-controlled low-GI meals. Observational and interventional studies have linked GI to the risk of obesity, diabetes, heart disease, and cancer, although the topic remains much debated. One factor contributing to this ongoing controversy is the relative paucity of data regarding the relevant molecular mechanisms. If differences in insulin secretion mediate the genetic effects observed by Kallio et al, similar effects would be expected to occur with both low-GI and high-GI diets. This possibility is supported by a human study and several rodent studies, which showed potentially beneficial changes in the expression of HSL and other relevant genes with a low-GI diet (8, 9)."

Contrastingly, the high-GI wheat (+oat+potato) diet upregulated 62 genes including those associated with activation of DEATH GENES:
-- Stress
-- Oxidative damage
-- Impaired immunity

So... high carb diet translates to... the equivalence of a STRESS RESPONSE. The authors discuss in more depth the results from the FUNGENUT Study..."Interestingly, the 12-wk oat-wheat-potato diet seemed to especially activate genes responding to stress. The oxidative stress pathway, interleukin pathway, and inflammation mediated by the chemokine and cytokine signaling pathway were also activated. Moreover, the present data suggest that the oat-wheat-potato diet, which induced repeated high insulin responses, can provoke alterations in immune status and inflammation. It is well established that adipose tissue has a role in inflammation (39). Cross-sectional epidemiologic data suggest that whole grains and a low-glycemic-index diet may reduce systemic inflammation in women with T2DM (40). Up-regulation of gene expression for serum and glucocorticoid-regulated kinase suggests activation of the glucocorticoid axis, which can occur in response to various stress stimuli (cytokines, aldosterone, growth factors, oxidative stress, heat shock protein activation, and glucocorticoids) (41). Activation of the pituitary-adrenal glucocorticoid axis may be involved in the pathogenesis of the metabolic syndrome (42)."

Dietary carbohydrate modification induces alterations in gene expression in abdominal subcutaneous adipose tissue in persons with the metabolic syndrome: the FUNGENUT Study.
Kallio P, et al.
Am J Clin Nutr. 2007 May;85(5):1169-70.
Department of Clinical Nutrition, Food and Health Research Centre, University of Kuopio, Kuopio, Finland.
BACKGROUND: Diets rich in whole-grain cereals and foods with a low glycemic index may protect against type 2 diabetes, but the underlying molecular mechanisms are unknown.
OBJECTIVE: The main objective was to test whether 2 different carbohydrate modifications--a rye-pasta diet characterized by a low postprandial insulin response and an oat-wheat-potato diet characterized by a high postprandial insulin response--affect gene expression in subcutaneous adipose tissue (SAT) in persons with the metabolic syndrome.
DESIGN: We assessed the effect of carbohydrate modification on SAT gene expression in 47 subjects [24 men and 23 women with a mean (+/-SD) age of 55 +/- 6 y] with the features of the metabolic syndrome in a parallel study design. The subjects had a mean (+/-SD) body mass index (kg/m(2)) of 32.1 +/- 3.8 and a 2-h plasma glucose concentration of 8.0 +/- 2.3 mmol/L. Adipose tissue biopsies were performed, and oral-glucose-tolerance tests and other biochemical measurements were conducted before and after the intervention.
RESULTS: We detected 71 down-regulated genes in the rye-pasta group, including genes linked to insulin signaling and apoptosis. In contrast, the 12-wk oat-wheat-potato diet up-regulated 62 genes related to stress, cytokine-chemokine-mediated immunity, and the interleukin pathway. The insulinogenic index improved after the rye-pasta diet (P=0.004) but not after the oat-wheat-potato diet. Body weight was unchanged in both groups.
CONCLUSIONS: Dietary carbohydrate modification with rye and pasta or oat, wheat, and potato differentially modulates the gene expression profile in abdominal subcutaneous adipose tissue, even in the absence of weight loss.
PMID: 17490981

These wonderful graphs from Finland researchers illustrate how the toxic effects of grain sources of carbohydrates occur when wheat and rye are fed to healthy volunteers. Above a glucose blood concentration of 150 mg/dl (=8.3 mmol/L), glucose starts to cause changes in protein folding and glycosylating proteins and tissues. Diabetes micro-vascular complications like eye/kidney/nerve ending damage are related to toxic concentrations of glucose. Imagine sugar coating the organs over time. The higher the concentration, the longer the duration, the more thicker and more damaging the sugar coating. Insulin is controlled by several factors. Food is one of the most potent controllers, with carbohydrates and their respective GIs raising insulin levels the most. Excessive insulin induces inflammation, which can progress and cause arterial stiffness, high blood pressure, Metabolic Syndrome, obesity, and also heart disease. Longevity has been associated with lower insulin levels. The below trial demonstrates the direct relationship in 18-year old men between fasting insulin and the existence of cardiovascular markers. The curves for low or no GI foods have no peaks and in comparison are relatively flat. Without a surge in insulin, inflammation is kept at bay.

Foods with no or little GI:
-- Non-starchy vegetables
-- Protein (tofu, meat, fish, etc)
-- Monounsaturated fat
-- Omega-3 PUFA
-- Saturated fat

The goal for an optimzed health status for nearly all metabolic and cardiovascular goals is NORMAL. Therefore the optimal range for insulin is as low as possible less than 5 - 10 mIU/L. The goal for glucoses pre-meal is less than 83 (=4.6mmol/L) and after meals less than 110 to 120 (=6.1 to 6.67mmol/L).

Relationship between fasting insulin and cardiovascular risk factors is already present in young men: the Verona Young Men Atherosclerosis Risk Factors Study.
Bonora E, et al. Eur J Clin Invest. 1997 Mar;27(3):248-54.
The associations between fasting plasma insulin concentration and risk factors for cardiovascular disease were examined in 979 18-year-old men participating in the Verona Young Men Atherosclerosis Risk Factors Study, a cross-sectional population-based study. Body mass index (BMI), waist-to-hip ratio (WHR), plasma triglycerides and uric acid concentrations, and blood pressure values significantly increased, and the high-density lipoprotein (HDL)-total cholesterol ratio decreased, across quartiles of fasting insulin. Total and low-density lipoprotein cholesterol, concentrations did not change significantly with the increase in fasting insulin levels. After adjustment for BMI, WHR, smoking, alcohol intake and physical activity, only plasma triglycerides significantly increased across insulin quartiles (F = 7.1; P less than 0.001). However, systolic blood pressure and uric acid were close to statistical significance (P = 0.06-0.07). Multiple linear regression analysis confirmed that plasma insulin was independently correlated with plasma triglycerides and, to a lesser extent, with blood pressure and uric acid concentration. This analysis pointed out that BMI was a stronger independent predictor of all cardiovascular disease risk factors than fasting insulin. When subjects were categorized according to the number of metabolic and haemodynamic disorders occurring within the same individual, subjects with multiple disorders (i.e, three or four) had higher plasma insulin levels than those with none or few disorders, even after adjusting for BMI, WHR and behavioural variables (F = 4.0; P less than 0.01). These results indicate that hyperinsulinaemia is already associated with a cluster of cardiovascular disease risk factors in young adulthood, the strongest independent association being with plasma triglycerides. PMID: 9088862

Tuesday, June 3, 2008

Wheat: Is It Evil Or Just in the Context of Vitamin D and EPA+DHA Deficiency?

I love Gladiator (yes, it's one of my all time f-a-v-e movies, next to When Harry Met Sally)... the first scene is mesmerizing... he's watching the flax and wheat fields glowing with gold, fearless in the face of death. In the dawn of time, ancient wheat probably did not cause as many autoimmune and silent/non-silent celiac diseases (or ?autism or ?coronary artery disease) as the present day. Why? In the Gladiator days, for one, sunscreen did not exist! Secondly, most people worked and warrior-ed outdoors. Toiling in the sun, hand laundering clothes, baking bread on outdoor hearths, practicing swordplay, gathering berries, fishing, preparing crops, hunting gamey-flesh (which BTW gamey-meat and grass-fed beef are enriched in EPA+DHA, much like fatty deep sea fish/fish oil), and other noble chores in the bright sunshine (because candles were scarce). All day long 24/7...

Does having enough sunlight and vitamin D give us more power to tolerate gluten and not develop damaging self-destructive auto-antibodies? It's unlikely we'll know in any good RCT (randomized controlled trials). No drug company will put up lettuce $$ to determine that good ol' cheap FREE UVB unblocked-sunshine is going to trump their $2-3/day drug (or super-sized vitamin D analogue) in a head-to-head trial. That's just absurd. And they're not stupid... because they pay staticians a lot of lettuce to figure that out for them.

Psoriasis is another celiac condition (incl autoimmune). What are the pharmacological treatments? UVB lightbox 5-10min weekly as needed and topical vitamin D derivatives in creams/ointments (and a couple of toxic Immunosuppressive injections like Enbrel for instance which has a side effect of c-a-n-c-e-r). New diagnostic techniques for celiac disease (widely used in Europe) are being employed now (check this out here). Years ago Dr. Davis figured out the value and power of oral administration of natural Vitamin D3. The recently published study impressively validates his work.

Effective tratment: Vitamin D3 (+ gluten-free lifestyle/diet plan)

Am J Med. 1978 Dec;65(6):1015-20.
Osteomalacia and celiac disease: response to 25-hydroxyvitamin D3. Hepner GW, Jowsey J, Arnaud C, Gordon S, Black J, Roginsky M, Moo HF, Young JF.
In this 54 year old woman with celiac disease, osteomalacia developed while she was on a gluten-free diet which had caused regression of her steatorrhea. She was not responsive to large doses of parenterally administered dihydrotachysterol (fake foreign synthetic vitamin D version) and calcium, but she was responsive to the oral administration of 25-hydroxyvitamin D3 (25-OHD3 = natural).

The data suggest that 25-OHD3 is the treatment of choice for patients with vitamin D deficiency due to intestinal malabsorption. PMID: 742623

Effective treatment: Fish oil!

Fish oil has been shown to be hugely beneficial due to its impressive autoimmune immunemodulating and skin-stabilizing benefits. Anything anti-inflammatory helps (like antioxidants with high ORAC scores). Fasting creates lower systemic bodily inflammation -- yes the MONKS know what they are doing. In TYP, the practice of intermittent fasting is a fast way to success.

Br J Dermatol. 2005 Oct;153(4):706-14.
Diet and psoriasis: experimental data and clinical evidence. Wolters M.

Psoriasis is considered as a T-cell-mediated inflammatory skin disease which is characterized by hyperproliferation and poor differentiation of epidermal keratinocytes. While susceptibility to psoriasis is inherited, the disease is influenced by environmental factors such as infections and stress. Diet has been suggested to play a role in the aetiology and pathogenesis of psoriasis. Fasting periods, low-energy diets and vegetarian diets improved psoriasis symptoms in some studies, and diets rich in n-3 polyunsaturated fatty acids from fish oil also showed beneficial effects. All these diets modify the polyunsaturated fatty acid metabolism and influence the eicosanoid profile, so that inflammatory processes are suppressed. Some patients with psoriasis show an elevated sensitivity to gluten. In patients with IgA and/or IgG antigliadin antibodies the symptoms have been shown to improve on a gluten-free diet. The active form of vitamin D, 1,25-dihydroxyvitamin D(3), exhibits antiproliferative and immunoregulatory effects via the vitamin D receptor (HOW ABOUT TAKING VITAMIN D3 ORALLY DAILY??), and thus is successfully used in the topical treatment of psoriasis. In this review, dietary factors which play a role in psoriasis are assessed and their potential benefit is evaluated. Furthermore, the risk of drug-nutrient interactions in psoriasis therapy is discussed (WOULDN'T IT BE NICE IF...SOMEDAY THEY SAY...WHEAT-CESSATION IS KEY TO PREVENTING PROGRESSION AND TO REVERSING PSORIASIS ?!?). PMID: 16181450

(These are many of the same strategies in TYP of course)

Are all autoimmune conditions (including Grave's and the frequently diagnosed Hashimoto's thyroiditis) just silent or non-silent celiac disease?

Why are wheat/gluten antibodies implicated so often?

Why is Vitamin D deficiency and a lack of dietary EPA+DHA commonly associated with celiac conditions (and autism and coronary artery disease)? And improve these conditions? Which came first? The chicken or the egg?? Does maternal health and in utero environments affect not only the fetus, but even the following generation as they do in rat experiments?

At least TrackYourPlaque provides answers.... Including the below...
--Optimize your vitamin D3 level (25)OHD = 60 ng/ml
--Optimize your fish oil EPA + DHA 3000 mg daily (supplements + dietary fish, shellfish, pasture-fed protein -- see last study) (or more if you have elevated Lp(a) > 30 mg/dl)
--Wheat-cessation program (yes.. that's all pasta, noodles, mac-n-cheese, bread, cereal, croissants (omg very hard), crackers, cookies, even soy sauce, etc)
--Optimize optimism (vitamin 'O')

Clin Rheumatol. 2006 Mar;25(2):240-5.
Association of systemic and thyroid autoimmune diseases.Biró E, Szekanecz Z, Czirják L, Dankó K, Kiss E, Szabó NA, Szucs G, Zeher M, Bodolay E, Szegedi G, Bakó G.

OBJECTIVE: There are few large cohort studies available on the association of systemic and thyroid autoimmune diseases. In this study, we wished to determine the association of Hashimoto's thyroiditis (HT) and Graves' disease (GD) with systemic autoimmune diseases.
METHODS: One thousand five hundred and seventeen patients with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), systemic sclerosis (SSc), mixed connective tissue disease (MCTD), Sjögren's syndrome (SS) and polymyositis/dermatomyositis (PM/DM) were included in the study. The HT and GD were diagnosed based on thorough clinical evaluation, imaging and fine-needle aspiration cytology (FNAC). The frequency of HT and GD in these diseases was assessed. In addition, 426 patients with HT or GD were assessed and the incidence of SLE, RA, SSc, MCTD, SS and PM/DM among these patients was determined. Prevalence ratios indicating the prevalences of GD or HT among our autoimmune patients in comparison to prevalences of GD or HT in the general population were calculated.

RESULTS: Altogether 8.2% of systemic autoimmune patients had either HT or GD. MCTD and SS most frequently overlapped with autoimmune thyroid diseases (24 and 10%, respectively). HT was more common among MCTD, SS and RA patients (21, 7 and 6%, respectively) than GD (2.5, 3 and 1.6%, respectively). The prevalences of HT in SLE, RA, SSc, MCTD, SS and PM/DM were 90-, 160-, 220-, 556-, 176- and 69-fold higher than in the general population, respectively. The prevalences of GD in the same systemic diseases were 68-, 50-, 102-, 76-, 74- and 37-fold higher than in the general population, respectively. Among all thyroid patients, 30% had associated systemic disease. In particular, 51% of HT and only 16% of GD subjects had any of the systemic disorders. MCTD, SS, SLE, RA, SSc and PM/DM were all more common among HT patients (20, 17, 7, 4, 2 and 2%, respectively) than in GD individuals (2, 5, 5, 1, 2 and 1%, respectively).
CONCLUSION: Systemic and thyroid autoimmune diseases often overlap with each other. HT and GD may be most common among MCTD, SSc and SS patients. On the other hand, these systemic diseases are often present in HT subjects. Therefore it is clinically important to screen patients with systemic autoimmune diseases for the co-existence of thyroid disorders. PMID: 16247581

Biomed Pharmacother. 2007 Feb-Apr;61(2-3):105-12.
Dietary omega-3 fatty acids for women. Bourre JM.

This review details the specific needs of women for omega-3 fatty acids, including alpha linoleic acid (ALA) and the very long chain fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).

Omega-3 fatty acid (dietary or in capsules) ensures that a woman's adipose tissue contains a reserve of these fatty acids for the developing fetus and the breast-fed newborn infant. This ensures the optimal cerebral and cognitive development of the infant. The presence of large quantities of EPA and DHA in the diet slightly lengthens pregnancy, and improves its quality. Human milk contains both ALA and DHA, unlike that of other mammals.
Conditions such as diabetes can alter the fatty acid profile of mother's milk, while certain diets, like those of vegetarians, vegans, or even macrobiotic diets, can have the same effect, if they do not include seafood.

ALA, DHA and EPA, are important for preventing ischemic cardiovascular disease in women of all ages.

Omega-3 fatty acids can help to prevent the development of certain cancers, particularly those of the breast and colon, and possibly of the uterus and the skin, and are likely to reduce the risk of postpartum depression, manic-depressive psychosis, dementias (Alzheimer's disease and others), hypertension, toxemia, diabetes and, to a certain extend, age-related macular degeneration.
Omega-3 fatty acids could play a positive role in the prevention of menstrual syndrome and postmenopausal hot flushes. The normal western diet contains little ALA (less than 50% of the RDA). The only adequate sources are rapeseed oil (canola; CAVEAT THIS ALSO CONTAINS OMEGA6'S WHICH IS PRO-INFLAMMATORY WHEN EXCESSIVE), walnuts and so-called "omega-3" eggs (similar to wild-type or Cretan eggs). The amounts of EPA and DHA in the diet vary greatly from person to person. The only good sources are fish and seafood, together with "omega-3" eggs. PMID: 17254747

Asia Pac J Clin Nutr. 2003.12 Suppl:S38
Feeding regimes affect fatty acid composition in Australian beef cattle. Mann NJ, Ponnampalam EN, Yep Y, Sinclair AJ.

Background - There is growing evidence that red meat contributes significantly to the intake of omega 3 long chain PUFA in western diets. The type of feeding regime used in animal production, can influence the lipids in red meat due to the fatty acid composition of the feed. Pasture feed being relatively rich in a-linolenic acid (18:3 n-3), while grain is relatively rich in linoleic acid (18:2n-6).
Objective - To determine the effect on beef fatty acid profile of varying length of grain feeding compared with grass feeding.
Design - Samples of rump, strip loin and blade cuts were obtained from eighteen cattle from each of three feeding regimes (pasture fed, short term grain feeding STGF, and long term grain feeding LTGF). All samples were analysed in triplicate as lean tissue only, using a standard chloroform - methanol extraction and capillary column gas-chromatograph fatty acid quantification.
Outcomes - Total fat, saturated and monounsaturated fatty acids were all significantly higher in the LTGF animals. The grass fed animals had higher levels of omega 3 PUFA in all three cuts, with combined EPA + DHA reaching levels in blade and strip loin that would meet Australian Food Standards classification as a ' source' of omega-3, with the rump cut reaching this level in the STGF group also. Rump from the grass fed animals was a relatively rich source of EPA + DHA and would qualify as a 'good source' of omega 3.
Conclusions - This study was able to show that pasture feeding of Australian cattle maximises omega-3 PUFA content and minimizes trans 18:1 fatty acid levels relative to grain feeding. Furthermore, LTGF results in elevated total fat and saturated fat content relative to STGF or grass feeding in lean cuts of Australian beef. PMID: 15023647