Tuesday, September 29, 2009

Sept. 29, 1898: Stalin’s Scientist Sees First Light | This Day In Tech | Wired.com

Sept. 29, 1898: Stalin’s Scientist Sees First Light | This Day In Tech | Wired.com

Early Soviet propagandists often relied on “miracles of science” to boost the status of their fledgling state. The young plant breeder Trofim Lysenko seemingly provided them with a whopper in 1927, reporting that he had developed a method of fertilizing fields without actually relying on fertilizers or minerals. The spinmeisters at Pravda had a field day, proclaiming that Lysenko had delivered on the Stalinist dream of using science to conquer nature.

Through a process he called “vernalization,” Lysenko reported growing peas in winter on the frozen steppe of Azerbaijan, causing Pravda to report breathlessly that Lysenko had turned …

the barren fields of the Trans-Caucasus green in winter, so that cattle will not perish from poor feeding, and the peasant Turk will live through the winter without trembling for tomorrow.

In fact, Lysenko’s methods were practically devoid of any science at all, and the “peasant Turk” continued to go hungry. But in a country where Joseph Stalin determined the truth and famine was ever present, the efficacy of vernalization was not to be denied. Top agricultural officials warmly embraced the process, and the tightly controlled state press dutifully pronounced it another miracle of Soviet science.

Except for the fact that crop vernalization didn’t work, it was, indeed, a miracle.

Lysenko’s star was definitely on the rise, thanks to officialdom’s alarming ability to ignore the facts in order to obtain the desired results. He also came to Moscow’s attention because of his talent for rallying the country’s peasantry, a surly segment of the population openly hostile to Stalinism. The hostility was thanks to Uncle Joe’s forced collectivization of small farms, which caused widespread starvation and the deaths of millions.

Lysenko, the semi-educated son of peasants, was able to put a human face on the regime back in the Kremlin. He spoke the peasants’ language and reassured them that science would fix everything.

He became a darling of Stalin’s, and after the dictator delivered a speech placing ideological needs above scientific research, Lysenko’s ascent was swift. In the early 1930s he was appointed head of the Academy of Agricultural Sciences and became the de facto arbiter of all the sciences, a mini-commissar, if you will. It was a catastrophe for Soviet science.

The little scientific theory absorbed by Lysenko came by way of Jean-Baptiste Lamarck, the early–19th-century French biologist who promulgated the theory, later refuted by Darwinism, that acquired characteristics could be passed from one generation to the next. This fit neatly with the Stalinist idea that nature could be manipulated to suit the needs of man.

Lysenko was hot-tempered, and he brooked no criticism of himself or his work. Legitimate Soviet geneticists and other scientists who dared oppose him often learned this hard truth with a one-way ticket to the gulag. Lysenko, in fact, despised his more-learned colleagues in a way that only a complete fraud with near-absolute power can.

He mercilessly rooted out perceived enemies of the state in what amounted to a crusade against science. With Stalin’s blessing, thousands of lab coats were shipped to Siberia, and hundreds died — or were killed — in the camps. In his own way, Lysenko proved to be as destructive to the Soviet Union as Stalin was with his purge of the Red Army officer corps.

For as long as Stalin lived, Lysenko was untouchable. After the dictator’s death in 1953, and his subsequent denunciation by Nikita Khrushchev at the 20th Communist Party Congress, Lysenko gradually lost influence. Although he held on to his offices for a time, scientists could now criticize him openly without fear of retribution. They did, with esteemed physicist Andrei Sakharov delivering the most withering blow in a 1964 address.

That same year, Lysenko saw his theories officially discredited and discarded by the Soviet Union. He was stripped of all his privileges, no small price to pay in Soviet society. In spite of everything, he kept showing up for work until his death in 1976.

Science thrown under the wagon in the name of politics. I think we're seeing similar things today, in terms of the "fat is bad for you" and "humans are warming the earth" theories. The government has already decided the answer to those two questions. Now do you want to help us save the world, or "confuse" people with contrary evidence?

Quest for a Long Life Gains Scientific Respect - NYTimes.com

Quest for a Long Life Gains Scientific Respect - NYTimes.com

Some attendees were so convinced of the virtues of less food that they have begun severe diets of various kinds. Cynthia Kenyon, of the University of California, San Francisco, said she had gone on a low-carb diet in 2002 after finding that food with even 2 percent sugar reduced the lifespan of the laboratory roundworms she studies. “Basically I try to steer clear of desserts and starches, though I do eat chocolate,” she said.

Her willowy figure makes her look at least a decade younger than her age.

from wikipedia...

Personal diet

Kenyon's research prompted her to make personal dietary changes. She stopped eating high glycemic index carbohydrates when she discovered that putting sugar on the worms' food shortened their lifespans.[1]

Kenyon follows a low glycemic index diet similar to the Atkins diet[1] and the South Beach Diet[2].

No desserts. No sweets. No potatoes. No rice. No bread. No pasta. When I say ‘no,’ I mean ‘no, or not much,’ she notes. Instead, eat green vegetables. Eat the fruits that aren't the sweet fruits, like melon. Bananas? Bananas are a little sweet. Meat? Meat, yes, of course. Avocados. All vegetables. Nuts. Fish. Chicken. That's what I eat. Cheese. Eggs. And one glass of red wine a day.[3]

I have a fabulous blood profile. My triglyceride level is only 30, and anything below 200 is good.[3]

You have to eat something, and you just have to make your best judgement. And that's my best judgement. Plus, I feel better. Plus, I'm thin—I weigh what I weighed when I was in college. I feel great —you feel like you're a kid again. It's amazing.[3]

In the past, Kenyon had also briefly experimented with a calorie restriction diet for two days, but couldn't stand the constant hunger.[1]

Interesting. Over time, it seems as if the antioxidant theory of aging is losing ground to the insulin theory of aging. This scientist is applying her research to her own health.

Friday, September 25, 2009

Cardiovascular Diabetology | Full text | Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study

Cardiovascular Diabetology | Full text | Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study

Results

Study participants had on average a diabetes duration of 9 years, a mean HbA1c of 6,6% units by Mono-S standard and were usually treated with metformin alone (3 subjects) or metformin in combination with a sulfonylurea (3 subjects) or a thiazolidinedione (3 subjects). Mean average dose of metformin was 1031 mg per day.

Compared to the diabetes diet, the Paleolithic diet resulted in lower mean values of
HbA1c (-0.4% units, p = 0.01),
triacylglycerol (-0.4 mmol/L, p = 0.003),
diastolic blood pressure (-4 mmHg, p = 0.03),
weight (-3 kg, p = 0.01), BMI (-1 kg/m2, p = 0.04) and waist circumference (-4 cm, p = 0.02), and
higher mean values of high density lipoprotein cholesterol (+0.08 mmol/L, p = 0.03).

The Paleolithic diet was mainly lower in cereals and dairy products, and higher in fruits, vegetables, meat and eggs, as compared with the Diabetes diet. Further, the Paleolithic diet was lower in total energy, energy density, carbohydrate, dietary glycemic load, saturated fatty acids and calcium, and higher in unsaturated fatty acids, dietary cholesterol and several vitamins. Dietary GI was slightly lower in the Paleolithic diet (GI = 50) than in the Diabetic diet (GI = 55).
Conclusion

Over a 3-month study period, a Paleolithic diet improved glycemic control and several cardiovascular risk factors compared to a Diabetes diet in patients with type 2 diabetes.

Men's Blood Pressure Increased By High-Sugar Diet

Men's Blood Pressure Increased By High-Sugar Diet

Study 1 highlights:

* Just two weeks on a high-fructose diet raises blood pressure in men.

* A drug used to treat gout seems to protect against that blood pressure increase and some aspects of metabolic syndrome.

Tuesday, September 22, 2009

Consumption of 2 and 4 egg yolks/d for 5 wk increases macular pigment concentrations in older adults with low macular pigment taking cholesterol-lower

Consumption of 2 and 4 egg yolks/d for 5 wk increases macular pigment concentrations in older adults with low macular pigment taking cholesterol-lowering statins -- Vishwanathan et al., 10.3945/ajcn.2009.28013 -- American Journal of Clinical Nutrition
ABSTRACT

Background: Lutein and zeaxanthin may reduce the risk of dry, age-related macular degeneration because of their photo-oxidative role as macular pigment.

Objective: The present study evaluated serum lutein, zeaxanthin, and macular pigment optical density (MPOD) responses at 0.25°, 0.5°, and 1° retinal eccentricities to the consumption of 2 and 4 egg yolks/d by older adults taking cholesterol-lowering medications.

Design: Subjects consumed foods containing 2 followed by 4 egg yolks/d for 5 wk each with a 4-wk egg-free period at baseline and between the 2 interventions.

Results: Changes in MPOD (n = 37) with egg yolk consumption were inversely associated (P < 0.05) with baseline MPOD. Subjects with low-baseline MPOD (defined as MPOD ≤0.5 at 0.25°, ≤0.4 at 0.5°, and ≤0.35 at 1°) showed increases of ≤50% (P < 0.05) with 4 egg yolks at the 3 retinal eccentricities. MPOD increased by 31% (P = 0.059) at 0.5° with 2 egg yolks. Serum lutein increased by only 16% and 24% (P < 0.05) compared with increases of 36% and 82% (P < 0.001) in serum zeaxanthin (n = 52) after consumption of 2 and 4 egg yolks, respectively. Serum HDL cholesterol increased by 5% (P < 0.05) after consumption of 2 and 4 egg yolks. Serum LDL cholesterol did not change with either egg yolk treatment.

Conclusions: Consumption of 4 egg yolks/d, and possibly of 2 egg yolks/d, for 5 wk benefited macular health in older adults with low MPOD. Serum HDL cholesterol increased without an increase in LDL cholesterol in this study population, most of whom were taking cholesterol-lowering statins.

Monday, September 14, 2009

low carb diet beats low fat for improving metabolic syndrome, again

SpringerLink - Journal Article

Abstract We recently proposed that the biological markers improved by carbohydrate restriction were precisely those that define the metabolic syndrome (MetS), and that the common thread was regulation of insulin as a control element. We specifically tested the idea with a 12-week study comparing two hypocaloric diets (~1,500 kcal): a carbohydrate-restricted diet (CRD) (%carbohydrate:fat:protein = 12:59:28) and a low-fat diet (LFD) (56:24:20) in 40 subjects with atherogenic dyslipidemia. Both interventions led to improvements in several metabolic markers, but subjects following the CRD had consistently reduced glucose (−12%) and insulin (−50%) concentrations, insulin sensitivity (−55%), weight loss (−10%), decreased adiposity (−14%), and more favorable triacylglycerol (TAG) (−51%), HDL-C (13%) and total cholesterol/HDL-C ratio (−14%) responses. In addition to these markers for MetS, the CRD subjects showed more favorable responses to alternative indicators of cardiovascular risk: postprandial lipemia (−47%), the Apo B/Apo A-1 ratio (−16%), and LDL particle distribution. Despite a threefold higher intake of dietary saturated fat during the CRD, saturated fatty acids in TAG and cholesteryl ester were significantly decreased, as was palmitoleic acid (16:1n-7), an endogenous marker of lipogenesis, compared to subjects consuming the LFD. Serum retinol binding protein 4 has been linked to insulin-resistant states, and only the CRD decreased this marker (−20%). The findings provide support for unifying the disparate markers of MetS and for the proposed intimate connection with dietary carbohydrate. The results support the use of dietary carbohydrate restriction as an effective approach to improve features of MetS and cardiovascular risk.

Diabetes of the Liver: The Link Between Nonalcoholic Fatty Liver Disease and High fructose corn syrup

Obesity - Abstract of article: Diabetes of the Liver: The Link Between Nonalcoholic Fatty Liver Disease and HFCS-55

Nonalcoholic fatty liver disease (NAFLD) is associated with obesity and insulin resistance. It is also a predisposing factor for type 2 diabetes. Dietary factors are believed to contribute to all three diseases. NAFLD is characterized by increased intrahepatic fat and mitochondrial dysfunction, and its etiology may be attributed to excessive fructose intake. Consumption of high fructose corn syrup-55 (HFCS-55) stands at up to 15% of the average total daily energy intake in the United States, and is linked to weight gain and obesity. The aim of this study was to establish whether HFCS-55 could contribute to the pathogenesis of NAFLD, by examining the effects of HFCS-55 on hepatocyte lipogenesis, insulin signaling, and cellular function, in vitro and in vivo. Exposure of hepatocytes to HFCS-55 caused a significant increase in hepatocellular triglyceride (TG) and lipogenic proteins. Basal production of reactive oxygen metabolite (ROM) was increased, together with a decreased capacity to respond to an oxidative challenge. HFCS-55 induced a downregulation of the insulin signaling pathway, as indicated by attenuated ser473phosphorylation of AKT1. The c-Jun amino-terminal kinase (JNK), which is intimately linked to insulin resistance, was also activated; and this was accompanied by an increase in endoplasmic reticulum (ER) stress and intracellular free calcium perturbation. Hepatocytes exposed to HFCS-55 exhibited mitochondrial dysfunction and released cytochrome C (CytC) into the cytosol. Hepatic steatosis and mitochondrial disruption was induced in vivo by a diet enriched with 20% HFCS 55; accompanied by hypoadiponectinemia and elevated fasting serum insulin and retinol-binding protein-4 (RBP4) levels.

Taken together our findings indicate a potential mechanism by which HFCS-55 may contribute to the pathogenesis of NAFLD.

ScienceDirect - Nutrition, Metabolism and Cardiovascular Diseases : Carbohydrate restriction favorably alters lipoprotein metabolism in Emirati subjects classified with the metabolic syndrome

ScienceDirect - Nutrition, Metabolism and Cardiovascular Diseases : Carbohydrate restriction favorably alters lipoprotein metabolism in Emirati subjects classified with the metabolic syndrome

Background and aims

Carbohydrate restriction (CR) has been shown to improve dyslipidemias associated with metabolic syndrome (MetS). We evaluated the effects of CR on lipoprotein subfractions and apolipoproteins in Emirati adults classified with the MetS.
Methods and results

39 subjects (15 men/24 women) were randomly allocated to a CR diet [20–25% energy from carbohydrate (CHO)] for 12 wk (CRD group) or a combination treatment consisting of CRD for 6 wk followed by the American Heart Association diet (50–55% CHO, AHA group) for an additional 6 wk. All subjects reduced body weight, LDL cholesterol and triglycerides (P < 0.01). At baseline all subjects had low concentrations of medium VLDL and total HDL particles associated with the very low plasma triglycerides and HDL cholesterol in this population. After 12 wk, the large VLDL subfraction was decreased over time for subjects in the CRD group (P < 0.01) while these changes were not observed in those subjects who changed to the AHA diet. The number of medium and small LDL particles decreased for all subjects rendering a less atherogenic lipoprotein profile. In agreement with these results, a significant decrease in apolipoprotein (apo) B was observed (P < 0.01). The medium HDL subfraction and apo A-II, which can be considered pro-atherogenic, were also decreased over time in the CRD group only.

Conclusions

These results suggest that weight loss favorably affects lipoprotein metabolism and that the CRD had a better effect on atherogenic VLDL and HDL than the low fat diet recommended by AHA.

Monday, September 07, 2009

High protein intake reduces intrahepatocellular lipid deposition in humans -- Bortolotti et al., 10.3945/ajcn.2008.27296 -- American Journal of Clinical Nutrition

High protein intake reduces intrahepatocellular lipid deposition in humans -- Bortolotti et al., 10.3945/ajcn.2008.27296 -- American Journal of Clinical Nutrition

Background: High sugar and fat intakes are known to increase intrahepatocellular lipids (IHCLs) and to cause insulin resistance. High protein intake may facilitate weight loss and improve glucose homeostasis in insulin-resistant patients, but its effects on IHCLs remain unknown.

Objective: The aim was to assess the effect of high protein intake on high-fat diet–induced IHCL accumulation and insulin sensitivity in healthy young men.

Increasing protein in the diet reduces the dangerous buildup of fat in the liver. This fatty liver problem is fond in alcoholics and people consuming large amounts of fructose, i.e. metabolic syndrome.

Access : Connecting obesity, aging and diabetes : Nature

Access : Connecting obesity, aging and diabetes : Nature:

"Obesity accelerates the aging of adipose tissue, a process only now beginning to come to light at the molecular level. Experiments in mice suggest that obesity increases the formation of reactive oxygen species in fat cells, shortens telomeres—and ultimately results in activation of the p53 tumor suppressor, inflammation and the promotion of insulin resistance (pages 1082–1087).

Obesity accelerates the aging of adipose tissue, leading to inflammation and insulin resistance.

As technology has improved hygiene, the food supply and living standards overall, there has been a rise in such age-related illnesses as cardiovascular disease, cancer, degenerative diseases of the brain and other organs, and metabolic disorders such as diabetes. Age-related disorders have become widespread throughout the world, replacing infectious diseases as the leading cause of death in developed countries."

Over 70% of American children deficient in vitamin D! - Kumar et al. 124 (3): e362 -- Pediatrics

Prevalence and Associations of 25-Hydroxyvitamin D Deficiency in US Children: NHANES 2001-2004 -- Kumar et al. 124 (3): e362 -- Pediatrics:

OBJECTIVES: To determine the prevalence of 25-hydroxyvitamin D (25[OH]D) deficiency and associations between 25(OH)D deficiency and cardiovascular risk factors in children and adolescents.

"CONCLUSIONS: 25(OH)D deficiency is common in the general US pediatric population and is associated with adverse cardiovascular risks."

Over 70% of American children deficient in vitamin D!

7 Reasons to Eat More Saturated Fat

7 Reasons to Eat More Saturated Fat


7 Reasons to Eat More Saturated Fat 108 Comments

Written by Tim Ferriss Topics: Physical Performance

7 Reasons to Eat More Saturated Fat

In the not-so-distant past, the medical establishment considered all fats equally loathsome: all fats were created equal and they’re all bad for you. Things have changed in that quarter, if only slightly. You have no doubt heard the drumbeat of current medical thinking on fats: some fats are now good for you—olive oil and canola oil*—but others are bad for you—trans fats and all saturated fats. That’s an improvement from the old cry, but far from the truth.

It seems that no matter how the story spins from the denizens of the anti-fat camp, one piece of their advice remains staunchly constant: “You should sharply limit your intake of saturated fats.” The next admonition will invariably be, “which have been proven to raise cholesterol and cause heart disease.” Their over-arching belief is that saturated fat is bad, bad, bad.

You see with just a glance at [our suggested meal plans] that we’ve included fatty cuts of meat, chicken with the skin, bacon, eggs, butter, coconut oil, organic lard, and heavy cream in the plan. Aren’t we worried that these foods will increase your risk of heart disease and raise your cholesterol? In a word, nope. In fact, we encourage you to make these important fats a regular part of your healthy diet. Why? Because humans need them and here are just a few reasons why.

1) Improved cardiovascular risk factors

Though you may not have heard of it on the front pages of your local newspaper, online news source, or local television or radio news program, saturated fat plays a couple of key roles in cardiovascular health. The addition of saturated fat to the diet reduces the levels of a substance called lipoprotein (a)—pronounced “lipoprotein little a” and abbreviated Lp(a)—that correlates strongly with risk for heart disease. Currently there are no medications to lower this substance and the only dietary means of lowering Lp(a) is eating saturated fat. Bet you didn’t hear that on the nightly news. Moreover, eating saturated (and other) fats also raises the level of HDL, the so-called good cholesterol. Lastly, research has shown that when women diet, those eating the greatest percentage of the total fat in their diets as saturated fat lose the most weight.

2) Stronger bones

In middle age, as bone mass begins to decline, an important goal (particularly for women) is to build strong bones. You can’t turn on the television without being told you need calcium for your bones, but do you recall ever hearing that saturated fat is required for calcium to be effectively incorporated into bone? According to one of the foremost research experts in dietary fats and human health, Mary Enig, Ph.D., there’s a case to be made for having as much as 50 percent of the fats in your diet as saturated fats for this reason. That’s a far cry from the 7 to 10 percent suggested by mainstream institutions. If her reasoning is sound—and we believe it is— is it any wonder that the vast majority of women told to avoid saturated fat and to selectively use vegetable oils instead would begin to lose bone mass, develop osteoporosis, and get put on expensive prescription medications plus calcium to try to recover the loss in middle age?

3) Improved liver health

Adding saturated fat to the diet has been shown in medical research to encourage the liver cells to dump their fat content. Clearing fat from the liver is the critical first step to calling a halt to middle-body fat storage. Additionally, saturated fat has been shown to protect the liver from the toxic insults of alcohol and medications, including acetaminophen and other drugs commonly used for pain and arthritis, such as nonsteroidal anti-inflammatory drugs or NSAIDs, and even to reverse the damage once it has occurred. Since the liver is the lynchpin of a healthy metabolism, anything that is good for the liver is good for getting rid of fat in the middle. Polyunsaturated vegetable fats do not offer this protection.

4) Healthy lungs

For proper function, the airspaces of the lungs have to be coated with a thin layer of what’s called lung surfactant. The fat content of lung surfactant is 100 percent saturated fatty acids. Replacement of these critical fats by other types of fat makes faulty surfactant and potentially causes breathing difficulties. Absence of the correct amount and composition of this material leads to collapse of the airspaces and respiratory distress. It’s what’s missing in the lungs of premature infants who develop the breathing disorder called infant respiratory distress syndrome. Some researchers feel that the wholesale substitution of partially hydrogenated (trans) fats for naturally saturated fats in commercially prepared foods may be playing a role in the rise of asthma among children. Fortunately, the heyday of trans fats is ending and their use is on the decline. Unfortunately, however, the unreasoning fear of saturated fat leads many people to replace trans fats with an overabundance of polyunsaturated vegetable oils, which may prove just as unhealthful.

5) Healthy brain

You will likely be astounded to learn that your brain is mainly made of fat and cholesterol. Though many people are now familiar with the importance of the highly unsaturated essential fatty acids found in cold-water fish (EPA and DHA) for normal brain and nerve function, the lion’s share of the fatty acids in the brain are actually saturated. A diet that skimps on healthy saturated fats robs your brain of the raw materials it needs to function optimally.

6) Proper nerve signaling

Certain saturated fats, particularly those found in butter, lard, coconut oil, and palm oil, function directly as signaling messengers that influence the metabolism, including such critical jobs as the appropriate release of insulin. And just any old fat won’t do. Without the correct signals to tell the organs and glands what to do, the job doesn’t get done or gets done improperly.

7) Strong immune system

Saturated fats found in butter and coconut oil (myristic acid and lauric acid) play key roles in immune health. Loss of sufficient saturated fatty acids in the white blood cells hampers their ability to recognize and destroy foreign invaders, such as viruses, bacteria, and fungi. Human breast milk is quite rich in myristic and lauric acid, which have potent germ-killing ability. But the importance of the fats lives on beyond infancy; we need dietary replenishment of them throughout adulthood, middle age, and into seniority to keep the immune system vigilant against the development of cancerous cells as well as infectious invaders.