Tuesday, July 24, 2012

The #1 Cause of Obesity: Insulin | DietDoctor.com

The #1 Cause of Obesity: Insulin | DietDoctor.com

Oh my god. This 3rd episode of “The Skinny on Obesity” may be the best short video on obesity I’ve seen. Not because dr Robert Lustig tells me something I didn’t already know, but because he explains it so crystal clear that a kid will understand.
Do you want people to understand the reason behind perhaps 90 percent of obesity epidemic? Spread this video. It needs to be seen by as many people as possible.


The bottom line is that the cause of garden-variety obesity is relatively simple: Excess (processed) carbs increases insulin which increases fat storage. Some bloggers on the internet have objections to this, but that does not change the facts.

Sunday, July 15, 2012

[Evaluation of biological and clinical ... [Rocz Panstw Zakl Hig. 2012] - PubMed - NCBI

[Evaluation of biological and clinical ... [Rocz Panstw Zakl Hig. 2012] - PubMed - NCBI

[Evaluation of biological and clinical potential of paleolithic diet].
[Article in Polish]
Kowalski LM, Bujko J.

Wydział Nauk o Zywieniu Człowieka i Konsumpcji Szkoła Główna Gospodarstwa Wiejskiego, Warszawa. lukasz_kowalski@sggw.pl

Accumulating evidences suggest that foods that were regularly consumed during the human primates and evolution, in particular during the Paleolithic era (2.6-0.01 x 10(6) years ago), may be optimal for the prevention and treatment of some chronic diseases. It has been postulated that fundamental changes in the diet and other lifestyle conditions that occurred after the Neolithic Revolution, and more recently with the beginning of the Industrial Revolution are too recent taking into account the evolutionary time scale for the human genome to have completely adjust. In contemporary Western populations at least 70% of daily energy intake is provided by foods that were rarely or never consumed by Paleolithic hunter-gatherers, including grains, dairy products as well as refined sugars and highly processed fats. Additionally, compared with Western diets, Paleolithic diets, based on recently published estimates of macronutrient and fatty acid intakes from an East African Paleolithic diet, contained more proteins and long-chain polyunsaturated fatty acids, and less linoleic acid. Observational studies of hunter-gatherers and other non-western populations lend support to the notion that a Paleolithic type diet may reduce the risk of cardiovascular disease, metabolic syndrome, type 2 diabetes, cancer, acne vulgaris and myopia. Moreover, preliminary intervention studies using contemporary diet based on Paleolithic food groups (meat, fish, shellfish, fresh fruits and vegetables, roots, tubers, eggs, and nuts), revealed promising results including favorable changes in risk factors, such as weight, waist circumference, C-reactive protein, glycated haemoglobin (HbAlc), blood pressure, glucose tolerance, insulin secretion, insulin sensitivity and lipid profiles. Low calcium intake, which is often considered as a potential disadvantage of the Paleolithic diet model, should be weighed against the low content of phytates and the low content of sodium chloride, as well as the high amount of net base yielding vegetables and fruits. Increasing number of evidences supports the view that intake of high glycemic foods and insulinotropic dairy products is involved in the pathogenesis and progression of acne vulgaris in Western countries. In this context, diets that mimic the nutritional characteristics of diets found in hunter-gatherers and other non-western populations may have therapeutic value in treating acne vulgaris. Additionally, more studies is needed to determine the impact of gliadin, specific lectins and saponins on intestinal permeability and the pathogenesis of autoimmune diseases.

High Triglycerides blunt leptin, causing hunger. Winning the Battle of the Bulge: We're a Scrimmage Closer to Victory | Saint Louis University

Winning the Battle of the Bulge: We're a Scrimmage Closer to Victory | Saint Louis University

April 27, 2004

Winning the Battle of the Bulge: We're a Scrimmage Closer to Victory
"We feel that we now understand what part of the system is broken -- why leptin isn't working." -- William A. Banks, M.D.

ST. LOUIS -- Saint Louis University researchers believe they've won a major skirmish in the battle of the bulge, and their findings are published in the May issue of Diabetes.

"We figured out how obesity occurs," says William A. Banks, M.D., professor of geriatrics in the department of internal medicine and professor of pharmacological and physiological science at Saint Louis University School of Medicine. "The next step is coming up with the solution."

The scientists used mice to look at how leptin, a hormone secreted by fat cells that tells us to stop eating, gets into the brain. They found that in obese mice, high triglycerides, a type of fat in the bloodstream, prevents leptin from getting into the brain, where it can do its work in turning off feeding and burning calories.

"High triglycerides are blocking the leptin from getting into the brain. If leptin can't get into the brain, it can't tell you to stop eating," says Banks, who is principal investigator and a staff physician at Veterans Affairs Medical Center in St. Louis.

"This is a big deal. We now know what is keeping leptin from getting to where it needs to do its work."

Paradoxically high triglycerides occur in both fat and starving animals and make the brain think the body's starving so the animal keeps eating, which makes it gain more weight.

I read this article and thought, wow, new discovery? But it sounded like something I read before. Viola, here's a Dr. Eades article from 5 years ago where he says the same thing. Some discovery. Oh, and of course the answer isn't to lower triglycerides through low carb diets, but to invent a new pill.

Leptin, low-carb and hunger

So as leptin levels wax and wane, so does your sense of hunger and even, to an extent, your metabolic rate.

Where does the low-carb diet fit into the picture?

There is a critical point in the cycle described above. That critical point is when the leptin crosses the BBB. If the leptin can’t get across the BBB, it can’t get to the brain. If it doesn’t get to the brain, it doesn’t shut off the hunger response irrespective of how much is circulating in the blood.

Most obese people find themselves in this very situation: high blood levels of leptin but still hungry. And eating makes more fat, which makes more leptin, which should shut off the hunger response, but it doesn’t because the ever increasing levels of leptin telling the brain to tell the obese person to quit eating don’t get to the brain to do their job.

Why not?

Research done a couple of years ago in St. Louis and in Japan pinpointed the problem. Triglycerides – fat circulating in the blood – interrupts the passage of leptin across the BBB. If trigylcerides are high, which they are in most obese people, then, basically, they block the movement of leptin into the brain. So, leptin levels are elevated in the blood, and triglycerides keep the leptin from getting to where it needs to get to shut off hunger. (click here for the abstract and full text of this research paper.)

We all know that the commonest lab finding in people following a low-carb diet is a dramatic reduction in triglyceride levels. This reduction in triglycerides allows the leptin that is already circulating in relatively large amounts to get through to the brain where it can reduce hunger. I believe that this reduction in triglycerides (which happens fairly quickly) is the primary reason that people substantially decrease their hunger on low-carb diets. And remember from the graphic above that leptin – once it gets to the brain – actually increases thermogenesis as well, which means that the metabolic rate increases.

Decreased absorption of calcium, magnesium, zinc and ... [J Nutr. 1976] - PubMed - NCBI

Decreased absorption of calcium, magnesium, zinc and ... [J Nutr. 1976] - PubMed - NCBI

J Nutr. 1976 Apr;106(4):493-503.
Decreased absorption of calcium, magnesium, zinc and phosphorus by humans due to increased fiber and phosphorus consumption as wheat bread.
Reinhold JG, Faradji B, Abadi P, Ismail-Beigi F.

During a 20 day period of high fiber consumption in the form of bread made partly from wheaten wholemeal, two men developed negative balances of calcium, magnesium, zinc and phosphorus due to increased fecal excretion of each element. The fecal losses correlated closely with fecal dry matter and phosphorus. Fecal dry matter, in turn, was directly proportional to fecal fiber excretion. Balances of nitrogen remained positive. Mineral elements were well-utilized by the same subjects during a 20-day period of white bread consumption.

Whole wheat bread causes mineral deficiencies? But the "Government Plate" tells me whole wheat foods are a health food? I'm so confused!

Intracellular magnesium and insulin resistance. [Magnes Res. 2004] - PubMed - NCBI

Intracellular magnesium and insulin resistance. [Magnes Res. 2004] - PubMed - NCBI

Intracellular magnesium and insulin resistance.
Takaya J, Higashino H, Kobayashi Y.

Department of Pediatrics, Kansai Medical University, Moriguchi, Osaka 570-8506, Japan. takaya@takii.kmu.ac.jp

Magnesium, the second most abundant intracellular divalent cation, is a cofactor of many enzymes involved in glucose metabolism. Magnesium has an important role in insulin action, and insulin stimulates magnesium uptake in insulin-sensitive tissues. Impaired biological responses to insulin is referred to as insulin resistance. This review was designed to reach a better understanding of the mechanism involved in the correlation between magnesium and insulin resistance. Intracellular magnesium concentration is low in type 2 diabetes mellitus and in hypertensive patients. In patients with type 2 diabetes an inverse association exists between the plasma magnesium and insulin resistance due to intracellular changes. The suppressed intracellular magnesium concentration may result in defective tyrosine kinase activity and modify insulin sensitivity by influencing receptor activity after binding or by influencing intracellular signaling and processing. Intracellular magnesium deficiency may affect the development of insulin resistance and alter the glucose entry into the cell.

CONCLUSIONS: Magnesium is required for both proper glucose utilization and insulin signaling. Metabolic alterations in cellular magnesium, which may play the role of a second messenger for insulin action, contribute to insulin resistance.