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Prevalence of CVD/Diabetes/MPB in South Asians

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Post  mphatesmpb Thu Jan 06, 2011 8:58 am

I figured that it might be a good idea to have a thread for discussing this particular topic. It seems like the diseases of modern civilization disproportionately affect South Asians. Hopefully we can gather some important information that will help us defeat MPB and the other metabolic disorders.
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Prevalence of CVD/Diabetes/MPB in South Asians Empty Fat oxidation, fitness and skeletal muscle expression of oxidative/lipid metabolism genes in South Asians: implications for insulin resistance?

Post  mphatesmpb Thu Jan 06, 2011 8:58 am


Abstract

BACKGROUND: South Asians are more insulin resistant than Europeans, which cannot be fully explained by differences in adiposity. We investigated whether differences in oxidative capacity and capacity for fatty acid utilisation in South Asians might contribute, using a range of whole-body and skeletal muscle measures.

METHODOLOGY/PRINCIPAL FINDINGS: Twenty men of South Asian ethnic origin and 20 age and BMI-matched men of white European descent underwent exercise and metabolic testing and provided a muscle biopsy to determine expression of oxidative and lipid metabolism genes and of insulin signalling proteins. In analyses adjusted for age, BMI, fat mass and physical activity, South Asians, compared to Europeans, exhibited; reduced insulin sensitivity by 26% (p = 0.010); lower VO2max (40.6±6.6 vs 52.4±5.7 ml x kg(-1) x min(-1), p = 0.001); and reduced fat oxidation during submaximal exercise at the same relative (3.77±2.02 vs 6.55±2.60 mg x kg(-1) x min(-1) at 55% VO2max, p = 0.013), and absolute (3.46±2.20 vs 6.00±1.93 mg x kg(-1) x min(-1) at 25 ml O(2) x kg(-1) x min(-1), p = 0.021), exercise intensities. South Asians exhibited significantly higher skeletal muscle gene expression of CPT1A and FASN and significantly lower skeletal muscle protein expression of PI3K and PKB Ser473 phosphorylation. Fat oxidation during submaximal exercise and VO2max both correlated significantly with insulin sensitivity index and PKB Ser473 phosphorylation, with VO2max or fat oxidation during exercise explaining 10-13% of the variance in insulin sensitivity index, independent of age, body composition and physical activity.

CONCLUSIONS/SIGNIFICANCE: These data indicate that reduced oxidative capacity and capacity for fatty acid utilisation at the whole body level are key features of the insulin resistant phenotype observed in South Asians, but that this is not the consequence of reduced skeletal muscle expression of oxidative and lipid metabolism genes.
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Prevalence of CVD/Diabetes/MPB in South Asians Empty I mentioned this in another thread, but for the sake of completion

Post  crincrin Thu Jan 06, 2011 11:25 am

Increased prevalence of insulin resistance and nonalcoholic fatty liver disease in Asian-Indian men. (HTG = hepatic triglyceride)

http://www.ncbi.nlm.nih.gov/pubmed/17114290

The prevalence of insulin resistance was approximately 2- to 3-fold higher in the Asian-Indians compared with all other ethnic groups, and this could entirely be attributed to a 3- to 4-fold increased prevalence of insulin resistance in Asian-Indian men

This increased prevalence of insulin resistance in the Asian-Indian men was associated with an approximately 2-fold increase in HTG content and plasma IL-6 concentrations compared with Caucasian men.

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Post  crincrin Thu Jan 06, 2011 12:03 pm

BTW, non-alcohol fatty liver disease (NAFLD) is considered the liver manifestation of metabolic syndrome. I believe fatty liver infiltrates were classically associated with alcoholism, and the non-alcohol associated version was characterized later, thus the nomenclature.

Steatohepatitis (inflammation of the liver) is the next step after fatty liver infiltrates. Then comes cirrhosis (fibrosis, scarring).

Fatty liver => steatohepatitis => cirrhosis
The above diseases can be associated with alcohol, or not associated with alcohol (thus the prefix NA for non-alcoholic).

Adiponectin is a hormone associated with insulin sensitivity. Its secreted by fat cells, but serum adiponectin decreases with body fat. So although fat cells secrete it, the more fat you have, the less adiponectin you have.




Serum adipokine profile in Indian men with nonalcoholic steatohepatitis: Serum adiponectin is paradoxically decreased in lean vs. obese patients

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B82Y0-4XJN7GR-1&_user=10&_coverDate=12/31/2009&_rdoc=1&_fmt=high&_orig=search&_origin=search&_sort=d&_docanchor=&view=c&_searchStrId=1597703803&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=bd73d3fec919ca7a8a33cd2a5929cf02&searchtype=a

In patients with NASH, adiponectin levels were lower than controls. Insulin Resistance as assessed by homeostasis model assessment (HOMA) was higher in obese than lean, NAFLD patients. Lean NAFLD patients had adiponectin levels lower than obese patients.

This paradoxical decrease of serum adiponectin as well as low frequency of insulin resistance in lean NAFLD suggests a possible different etiology for this subset of patients.

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Post  mphatesmpb Thu Jan 06, 2011 12:06 pm

CS,

When discussing your theories on other threads, you've mentioned improving the efficiency of cellular respiration.

What do you make of this idea that "reduced oxidative capacity and capacity for fatty acid utilisation at the whole body level are key features of the insulin resistant phenotype observed in South Asians?"

The problem seems to be rooted in genetics, as there are clearly differences in the expression of genes involving lipid metabolism and insulin sensitivity. You've mentioned epigenetics, and the possibility of "silencing" genes. Do you have any recommendations that might help individuals with the genetic issues mentioned in the article?

I've read on Mercola's website that weight training improves insulin sensitivity of cells composing skeletal muscle. I've also read that the efficiency of cellular respiration is dependent on cellular oxygen supply. Do you think exercise-induced angiogenesis (facilitating increased oxygen supply to the body's cells) would counteract the metabolic issues?

-MP
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Post  mphatesmpb Thu Jan 06, 2011 12:27 pm

crincrin,

I was reading through the study that you posted, and I had to look up "intramyocellular lipids." I found this study, which presents some interesting ideas connecting the study on non-alcoholic fatty liver disease to the one i posted about compromised cellular respiration in South Asian men:


Intramyocellular lipid content in human skeletal muscle.
Schrauwen-Hinderling VB, Hesselink MK, Schrauwen P, Kooi ME.
Department of Radiology, University Hospital Maastricht, P.O. Box 5800, 6202 AZ Maastricht, The Netherlands. vhi@rdia.azm.nl
Abstract
Fat can be stored not only in adipose tissue but also in other tissues such as skeletal muscle.
Fat droplets accumulated in skeletal muscle [intramyocellular lipids (IMCLs)] can be quantified by different methods, all with advantages and drawbacks. Here, we briefly review IMCL quantification methods that use biopsy specimens (biochemical quantification, electron microscopy, and histochemistry) and non-invasive alternatives (magnetic resonance spectroscopy, magnetic resonance imaging, and computed tomography).
Regarding the physiological role, it has been suggested that IMCL serves as an intracellular source of energy during exercise. Indeed, IMCL content decreases during prolonged submaximal exercise, and analogously to glycogen, IMCL content is increased in the trained state.
In addition, IMCL content is highest in oxidative, type 1 muscle fibers. Together, this, indeed, suggests that the IMCL content is increased in the trained state to optimally match fat oxidative capacity and that it serves as readily available fuel. However, elevation of plasma fatty acid levels or dietary fat content also increases IMCL content, suggesting that skeletal muscle also stores fat simply if the availability of fatty acids is high. Under these conditions, the uptake into skeletal muscle may have negative consequences on insulin sensitivity. Besides the evaluation of the various methods to quantify IMCLs, this perspective describes IMCLs as valuable energy stores during prolonged exercise, which, however, in the absence of regular physical activity and with overconsumption of fat, can have detrimental effects on muscular insulin sensitivity.
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Post  Guest Thu Jan 06, 2011 7:01 pm

http://jmm.sgmjournals.org/cgi/reprint/47/10/907.pdf


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Post  empty Fri Jan 07, 2011 4:15 am

A few questions before you guys go any further:

1. How do you define "South Asian"? Ethnic background, genetic similarity, or people living in South Asia?

2. Does your group, as defined above, show the same effects when placed in a different environment (ie they move somewhere across the globe)?


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Post  mphatesmpb Mon Jan 10, 2011 12:50 pm

empty,

You asked what I'd meant by "South Asians." When creating this thread, I guess I meant people from the Indian subcontinent.

From what I've observed, Indian men seem to exhibit the same rates of hair loss after moving to Western countries. It seems plausible that the widespread consumption of high-glycemic and processed foods, combined with lack of exercise, would exacerbate the genetic component of MPB.

-MP
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Post  mphatesmpb Thu Jul 14, 2011 10:38 am


Asian Indians who immigrate to northern Europe have lower serum 25-hydroxyvitamin D [25(OH)D] than Caucasians, and they develop vitamin D deficiency, rickets, and osteomalacia. We investigated vitamin D metabolism, the effects of 25(OH)D3 on vitamin D metabolism and activity of 25(OH)D-24-hydroxylase, the rate-limiting enzyme for degradation of 25(OH)D, from cultured skin fibroblasts of Asian Indians and compared them with cultured skin fibroblasts of Caucasians in the southern United States. Normal subjects, ages 20–40 yr, were admitted to a metabolic ward for 2.5 days and given a daily diet containing 400 mg calcium and 900 mg phosphorus. Serum vitamin D, serum 25(OH)D, urinary calcium, and urinary phosphorus were significantly lower, whereas serum immunoreactive intact parathyroid hormone (PTH) and serum 1,25-dihydroxy vitamin D[ 1,25(OH)2D] were significantly higher in Asian Indians than in Caucasians. Administration of 25(OH)D3 increased serum 25(OH)D and urinary calcium but did not change serum PTH or serum 1,25(OH)2D in Asian Indians. In cultured skin fibroblasts, Emax and Vmax of 25(OH)D-24-hydroxylase activity were significantly higher in Asian Indians. In summary, in Asian Indians serum vitamin D and 25(OH)D are markedly reduced, altered vitamin D metabolism is only partially reversed by 25(OH)D3, and 25(OH)D-24-hydroxylase activity in cultured skin fibroblasts is markedly increased. Thus, Asian Indians residing in the U.S. are at risk for developing vitamin D deficiency, rickets, and osteomalacia.
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Post  a<r Thu Jul 14, 2011 11:17 am

My Girlfriend loves indian food, so we've been cooking some recently.

Holy Shit.

I am nowhere near assumptive and I'm sure the very traditional indian food is better for you, but look at the common recipes.

Vegetable oils I'm noticing most often, TONS of wheat, most things are fried, spices which are very bad for hair, a lot of sugar, etc.

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Post  mphatesmpb Thu Jul 14, 2011 12:53 pm

I'm confused as to why 1,25(OH)2D is higher in South Asians. Since 1.25(OH)2D is the physiologically active form of vitamin D that is released by the kidneys, the study seems to show that Indians are actually less vitamin D deficient than are Caucasians. But of course nothing in biology is as simple as 1+1=2.
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Post  abc123 Thu Jul 14, 2011 1:31 pm

a<r wrote:My Girlfriend loves indian food, so we've been cooking some recently.

Holy Shit.

I am nowhere near assumptive and I'm sure the very traditional indian food is better for you, but look at the common recipes.

Vegetable oils I'm noticing most often, TONS of wheat, most things are fried, spices which are very bad for hair, a lot of sugar, etc.

Most meals are fried, but now ghee is replaced with vegetable oils. They are essentially eating southern america style lol. Traditional indian diet also sounds low in choline.

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Post  a<r Thu Jul 14, 2011 1:51 pm

^ Absolutely ... its actually shocking. Another surprise is how overly cooked the meat is, can't be very little benefit left to it by the time it gets in your mouth. Dripping and bloody for me please.

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Post  abc123 Thu Jul 14, 2011 2:19 pm

a<r wrote:^ Absolutely ... its actually shocking. Another surprise is how overly cooked the meat is, can't be very little benefit left to it by the time it gets in your mouth. Dripping and bloody for me please.

I agree, derailing the thread a little:

Diet of raw eggs, raw milk, barely cooked meat seems to be getting proven slowly. Maybe Aajonus Vonderplanitz is not so crazy...Just recently:

Abstract

Laying hens are known to be able to “bio-convert” health-promoting components from the diet into eggs. Wheat and corn are important sources of antioxidant phenolics in the human diet. Given the fact that wheat and corn are major feed ingredients of laying hens in Canada, the objectives of this study were to characterise the presence of novel phenolic compounds in egg yolk and to determine the effect of cooking methods on their content and activity. The total phenolic content of yolk extracts was 3.83 and 3.49μmol gallic acid equivalents/g dry yolk for wheat-based and corn-based yolks, respectively. Antioxidant properties of yolk extracts were measured by the ORAC, DPPH and ABTS assays. ORAC values were 151.1±26.1 and 155.9±9.5μmolTE/g for wheat-based and corn-based yolks, respectively. All cooking methods significantly reduced (p<0.05) the antioxidant values. Ferulic acid was detected in trace amounts and no other phenolic compounds were found. However, tryptophan and tyrosine were found to be two main contributors to the antioxidant property of egg yolk. The contents of total free amino acids were 10081.0 and 10009.5μg/g in wheat-based and corn-based yolks, respectively; cooking methods were found to reduce significantly the amount of free amino acids.

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Post  a<r Thu Jul 14, 2011 2:45 pm

Raw organic farm eggs are fantastic, have them often, have never been able to source raw milk though ...

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Post  mphatesmpb Thu Jul 14, 2011 3:35 pm


Traditional indian diet also sounds low in choline.

I think it's also low in vitamin C.

South Indians eat rice instead of wheat, and also consume plenty of turmeric.

Something else that's worth noting...during the last several decades coconut oil has largely been replaced by sesame oil. In fact in my native language sesame oil is called the "good oil." Supposedly there's some natural preservative in sesame seeds which allows the oil to remain unspoiled at room temperature, similar to olive oil. But I doubt the omega-6 fatty acids would be spared by high cooking temperatures.
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Post  9rugrats5 Thu Jul 14, 2011 5:50 pm

mphatesmpb wrote:

Traditional indian diet also sounds low in choline.

I think it's also low in vitamin C.

South Indians eat rice instead of wheat, and also consume plenty of turmeric.

Something else that's worth noting...during the last several decades coconut oil has largely been replaced by sesame oil. In fact in my native language sesame oil is called the "good oil." Supposedly there's some natural preservative in sesame seeds which allows the oil to remain unspoiled at room temperature, similar to olive oil. But I doubt the omega-6 fatty acids would be spared by high cooking temperatures.

A good topic going here. Regarding oils, extolling sesame oil is not a new phenomenon. Sesame oil is highly praised in old ayurvedic texts, probably more so than any other oil. If you notice oil based medicines in ayurvedic formulations, many are prepared in sesame oil.

For cooking purposes, one has to keep in mind that in old times, the oils produced were organic, limited in quantity, seasonal and fresh. Also, high heat cooking was usually not possible in earthern stoves fired by wood and twigs. Chances are, oil was not spoiled (or not spoiled much) in such cooking. Then different oils were used for cooking in different regions and also dependent on seasons. Coconut, sesame, mustard have all been traditionally used for cooking purposes. Still, I believe, that one of the most preferred medium was cow ghee, rather than vegetable oils.

The problem with the modern Indian diet is the same as everywhere else. Refined and polished grains, devoid of most fibres and minerals; use of faster yield varieties; pesticides. Even rice prepared in many places in India has the nutrition laden 'starch' thrown off as the refined palate likes its rice dry and fluffy!

Edit- And the famous Indian sweets! Let us remember that in old times, the sweets were made with ghee and cow milk, nutritious flours, and jaggery or unrefined sugarcane juice as sweetener. Compare this with today's sweets- made using vegetable oils (despite all claims by vendors), white sugar, refined white flours and processed buffalo milk. Why would anyone in their right minds touch the shop made sweets even with a barge pole?
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Post  mphatesmpb Fri Jul 15, 2011 3:59 am


For cooking purposes, one has to keep in mind that in old times, the oils produced were organic, limited in quantity, seasonal and fresh. Also, high heat cooking was usually not possible in earthern stoves fired by wood and twigs. Chances are, oil was not spoiled (or not spoiled much) in such cooking. Then different oils were used for cooking in different regions and also dependent on seasons. Coconut, sesame, mustard have all been traditionally used for cooking purposes. Still, I believe, that one of the most preferred medium was cow ghee, rather than vegetable oils.

Not just that, but refrigerators weren't available until relatively recent times. If saving food through refrigeration is not possible, you must consume the food immediately after preparation. Levels of lipid peroxides in cooked foods have been shown to increase with respect to time, even when the food is stored in the refrigerator. It's one thing to use vegetable oils in cooking...and something else entirely when you eat the food several weeks later. With the advent of large scale production of processed/packaged foods, you can imagine the amount of toxic byproducts are in the food by the time it reaches the consumer

Although there is a natural tendency to trust ancient medicinal systems like ayuerveda, we should remember that it's quite possible that many of those beliefs might have been mistaken. For example, many therapies in Siddha medicine involve administration of mercury...
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Post  a<r Fri Jul 15, 2011 5:26 am

Just want to note that Milk Cake with Cardamom is probably the best tasting thing in the world.

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Post  9rugrats5 Fri Jul 15, 2011 7:23 am

mphatesmpb wrote:

Not just that, but refrigerators weren't available until relatively recent times. If saving food through refrigeration is not possible, you must consume the food immediately after preparation. Levels of lipid peroxides in cooked foods have been shown to increase with respect to time, even when the food is stored in the refrigerator. It's one thing to use vegetable oils in cooking...and something else entirely when you eat the food several weeks later. With the advent of large scale production of processed/packaged foods, you can imagine the amount of toxic byproducts are in the food by the time it reaches the consumer

Spot on. And then there're the packaged microwaveable dinners.


Although there is a natural tendency to trust ancient medicinal systems like ayuerveda, we should remember that it's quite possible that many of those beliefs might have been mistaken. For example, many therapies in Siddha medicine involve administration of mercury...

Ayurveda classifies mercury as a rejuvenator. This does fly in the face of current accepted wisdom. I do not personally know what to think of it, but it may be the case that nowadays mercury is portrayed as a bigger villain than it might be. Weston Price Foundation people claim that if the body is healthy in the first place, and the gut and immunity functioning, excess of toxins like mercury are easily filtered by the body, and seafood can be safely taken by such healthy individuals.
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Post  a<r Fri Jul 15, 2011 7:54 am

I believe fully that Westonprice is right, otherwise everybody with fillings would succumb in a more similar manner to the same illnesses, but what we see is that healthy people often times remain healthy for a very long time even with fillings.

Mercury used to be a remedy called quicksilver. It worked on the same idea as most other allopathic "cures", it silences our bodies defences.

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Post  mphatesmpb Fri Jul 15, 2011 4:17 pm


Refined grain consumption and the metabolic syndrome in urban Asian Indians (Chennai Urban Rural Epidemiology Study 57

Abstract

The objective of the study was to evaluate the association of refined grains consumption with insulin resistance and the metabolic syndrome in an urban south Indian population. The study population comprised 2042 individuals aged ≥20 years randomly selected from the Chennai Urban Rural Epidemiology Study (CURES), a cross-sectional study on a representative population of Chennai, southern India. The metabolic syndrome was defined according to modified Adult Treatment Panel III guidelines; and insulin resistance, by the homeostasis assessment model. The mean refined grain intake was 333 g/d (46.9% of total calories) in this population. After adjustment for age, sex, body mass index, metabolic equivalent, total energy intake, and other dietary factors, higher refined grain intake was significantly associated with higher waist circumference (8% higher for the highest vs the lowest quartile, P for trend < .0001), systolic blood pressure (2.9%, P for trend < .0001), diastolic blood pressure (1.7%, P for trend = .03), fasting blood glucose (7.9%, P for trend = .007), serum triglyceride (36.5%, P for trend < .0001), low high-density lipoprotein cholesterol (−10.1%, P for trend < .0001), and insulin resistance (13.6%, P < .001). Compared with participants in the bottom quartile, participants who were in the highest quartile of refined grain intake were significantly more likely to have the metabolic syndrome (odds ratio, 7.83; 95% confidence interval, 4.72-12.99). Higher intake of refined grains was associated with insulin resistance and the metabolic syndrome in this population of Asian Indians who habitually consume high-carbohydrate diets.
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Post  Paradox Fri Jul 15, 2011 6:09 pm

aI believe fully that Westonprice is right, otherwise everybody with fillings would succumb in a more similar manner to the same illnesses, but what we see is that healthy people often times remain healthy for a very long time even with fillings.

Mercury used to be a remedy called quicksilver. It worked on the same idea as most other allopathic "cures", it silences our bodies defences.

a

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Post  crincrin Sun Aug 21, 2011 11:31 am

So how have you guys done on iodine?

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