Raise a Smarter Child by Kindergarten
Raise a Smarter Child by Kindergarten
by David Perlmutter, MD, FACN, ABIHM
The Better Brain Book


by David Perlmutter, MD, FACN, ABIHM

Coffee, Tea May Stall Diabetes

December 15th, 2009

Every Cup of Coffee Per Day Lowers Risk of Type 2 Diabetes by 7%

From WebMD.com:

Every cup of coffee a person drinks per day may lower the risk of diabetes by 7%.

A new review of research on the link between lifestyle factors, like coffee and tea consumption, and diabetes risk suggests that drinking regular or decaffeinated coffee and tea all lower the risk of type 2 diabetes.

Researchers say the number of people with type 2 diabetes is expected to increase by 65% by 2025, reaching an estimated 380 million people worldwide.

“Despite considerable research attention, the role of specific dietary and lifestyle factors remains uncertain, although obesity and physical inactivity have consistently been reported to raise the risk of diabetes mellitus,” write researcher Rachel Huxley, DPhil, of the George Institute for International Health, University of Sydney, Australia, and colleagues in the Archives of Internal Medicine.

They say several studies have suggested that drinking coffee may lower the risk of developing type 2 diabetes and others have shown that decaffeinated coffee and tea may offer similar benefits, but there has not been a recent review of the research on the issue.

In the study, researchers analyzed information from 18 studies on coffee and diabetes and another 13 studies that included data on decaffeinated coffee and tea drinking and diabetes. Overall, the studies involved nearly a million participants.

The results showed that people who drink more coffee, whether it’s regular or decaffeinated, or tea appear to have a lower risk of developing type 2 diabetes.

When the information from the individual studies was combined, researchers found each additional cup of coffee drunk per day was associated with a 7% lower risk of diabetes. People who drank three to four cups per day had about a 25% lower risk than those who drank two or fewer cups per day.

The study also showed that people who drank more than three to four cups of decaffeinated coffee per day had about a one-third lower risk of developing type 2 diabetes than those who didn’t drink any.

Tea drinkers who drank more than three to four cups of tea per day had about a one-fifth lower risk of diabetes than those who didn’t drink tea.

Researchers say the protective effect of coffee and tea drinking appears to be independent of other potentially confounding lifestyle factors and raises the possibility that something in the beverages has a direct biological effect on lowering the risk of type 2 diabetes.

Compounds in coffee and tea, such as magnesium and antioxidants, may also be involved and merit further research.

If such beneficial effects observed in interventional trials are real, “the implications for the millions of individuals who have diabetes mellitus, or who are at future risk of developing it, would be substantial,” the researchers write. “For example, the identification of the active components of these beverages would open up new therapeutic pathways for the primary prevention of diabetes mellitus. It could also be envisaged that we will advise our patients most at risk for diabetes mellitus to increase their consumption of tea and coffee in addition to increasing their levels of physical activity and weight loss.”

Insulin Resistance Linked to Protein ‘Signature’

April 10th, 2009

From MedpageToday.com:

Eating a lot of fat can lead to insulin resistance but, surprisingly, so will adding meat-based protein to the diet.


Action Points

Explain to interested patients that the adverse impact of a high-fat diet on insulin sensitivity is well known.

Note that this study suggests that a diet including fat and branched-chain amino acids — found in dairy product and meats — may also induce insulin resistance.
That’s the implication of a range of observations in lean and obese humans, followed by experiments in rats, according to Christopher Newgard, Ph.D., of Duke University Medical Center in Durham, N.C., and colleagues.

The human studies showed that obese people had several metabolic differences from their leaner counterparts, including increased levels of the so-called branched-chain amino acids leucine, isoleucine and valine, Dr. Newgard and colleagues wrote in the April issue of Cell Metabolism.

Those amino acids — some of the 20 building blocks of protein — are found in large amounts in dairy products and red meat.

The animal studies showed that rats fed a diet high in fat and branched-chain amino acids gained only a little more weight than animals fed a normal chow diet, while those on a high-fat diet only gained significantly more.

But the rats eating fat and protein were as insulin resistant as the animals fed a high-fat diet.

“Insulin resistance occurred in animals with a diet high in the branched-chain amino acids, but only if they were ingested along with a high level of fat in the diet,” Dr. Newgard said in a statement.

But, he added, “I want to be clear that our animal data suggest that there is nothing wrong with obtaining protein from sources that are high in branched-chain amino acids, as long as you are not eating beyond what your energy needs are.”

Problems may arise, though, “if you add a lot of unneeded protein to a fatty diet,” he said. “The ancient Greeks were right: everything in moderation.”

The researchers set out to understand metabolic, endocrine, inflammatory, and physiologic differences between obese and lean subjects.

In a cohort of 73 obese and 67 lean volunteers, they measured 19 hormones involved in energy balance and fuel homeostasis, four pro- and anti-inflammatory cytokines, variables such as insulin sensitivity, body composition, and resting metabolic rate, and a range of more than 100 metabolites.

As expected, the obese volunteers were significantly less insulin sensitive than their lean counterparts. The homeostasis model assessment (HOMA) index was 2.3 times higher than in lean controls, which was significant at P0.0001.

And in a subset of participants who had intravenous glucose tolerance testing, the insulin sensitivity index was 2.1-fold higher in lean subjects, which was significant at P0.001.

But the key finding was that obese volunteers had a “signature” — consisting of branched-chain amino acids and their metabolites — that was significantly associated with a higher HOMA index (at P0.001).

Because of that observation, Dr. Newgard and colleagues fed rats on three different diets — a standard chow, a high-fat diet, and a diet high in fat and branched-chain amino acids.

After 13 weeks, the high-fat rats were 70% heavier than they were at the start, compared with 51% and 49% for the fat/protein and standard chow animals, respectively. The difference between the high-fat group and the others was significant at P0.039.

The difference in weight gain between the two high-fat groups was mainly caused by rates of food intake — rats in the high-fat group ate an average of 746 kilocalories a week compared with 666 for the animals getting fat and protein. (The chow-fed rats averaged 782 kilocalories a week, but were more active than the fat/protein animals, accounting for the similar weight gain.)

The fat/protein group had increases of up to 150% in leucine and isoleucine and 109% in valine, compared with the other two groups.

Despite gaining weight at a rate similar to the chow-fed animals, the rats fed high fat and protein were as insulin resistant (on glucose and insulin tolerance tests) after 15 weeks as the high-fat-fed animals.

To rule out the possibility that it was the fat and not the branched-chain amino acids that were responsible, the researchers conducted a second feeding test.

Three groups of animals were allowed to feed at will on standard chow, a high-fat diet, and a high-fat diet with additional branched-chain amino acids.

A fourth group was fed a high-fat diet, but only allowed to eat as much as their counterparts in the high-fat/protein group.

As expected, the fourth group had body weights identical to the high-fat/protein group and not significantly different from the chow-fed animals.

But intravenous glucose tolerance testing showed clear insulin resistance in the high-fat and fat/protein group, but not in the other two groups, demonstrating that moderate fat intake is not enough to induce insulin resistance, the researchers said.

Dr. Newgard and colleagues said more research is needed before dietary advice can be given but, overall, the results suggest that “in the context of a dietary pattern that includes high-fat consumption, (food containing branched-chain amino acids) may make an independent contribution to development of insulin resistance and diabetes.”

Acetyl L-Carnitine – What You Need to Know

January 24th, 2009

By David Perlmutter, MD, FACN, ABIHM

L-Carnitine is truly a mind-body nutrient. Found in all cells of the body and brain, L-carnitine has three main functions. First it transports long chain fatty acids across the inner membrane of the mitochondria. There the fats enter the citric acid cycle to be converted to ATP, the “energy molecule” needed by every cell to carry out its myriad activities. Muscle cells, heart cells and liver cells have very high numbers of mitochondria and correspondingly high amounts of carnitine.(1)

Second, L-carnitine acts as an antioxidant to protect cells from damage by free-radicals in the body and brain. In doing this, L-carnitine reduces the metabolic waste products that damage cells over time. Third, acetyl-L-carnitine donates its acetyl group to a choline molecule in a process that produces the neurotransmitter acetylcholine, which is actively involved in learning and memory.
Here’s a bit about different names for carnitine. Like many molecules in nature, carnitine is found in two stereoisomer forms, literally a “right-handed” shape (D-form) and a “left-handed” shape (L-form). Only the L-form, L-carnitine — also known as levocarnitine — is active. Much current research is done with the activated form, acetyl-L-carnitine, also called ALC or ALCAR.(1) Activated forms of substances in the body are the final molecules needed to carry out any specific activity.

Sources of L-carnitine include biosynthesis in the body, foods, and supplements. Made in the liver and kidney from the amino acids lysine and methionine, the biosynthesis of carnitine requires iron and vitamins C, B-6, and niacin. Acetyl-L-carnitine is made in small amounts naturally in the body, but, as is true of so many substances in the body, its production begins to decline in midlife.(2)

Carnitine is found primarily in animal foods. A 3.5 ounce portion of beef steak, pork, cod, and chicken breast contain 95 mg, 28 mg, 6 mg, and 4 mg respectively. Other sources of L-carnitine include over-the-counter vitamins, energy drinks, and various other products. Interestingly products containing L-carnitine cannot be marketed as “natural health products” in Canada and are not allowed to be imported into Canada.(3)

Because of L-carnitine’s vital roles in energy production and anti-oxidant capabilities, it has beneficial effects on a wide variety of health conditions. Clinical applications of L-carnitine include: diabetes (4); weight loss; enhanced male fertility; enhanced physical performance; and cognitive functioning.

A study done in Italy evaluated the efficacy of L-carnitine on physical and mental fatigue, and on cognitive functions of 66 centenarians. Thirty-two received 2,000 mg levocarnitine daily and 34 received a placebo for 6 months. Changes were monitored in total fat mass, total muscle mass, serum triacylglycerol, total cholesterol, HDL cholesterol, LDL cholesterol, Mini-Mental State Examination (MMSE), Activities of Daily Living, and a 6-min walking corridor test. Researchers concluded that “oral administration of levocarnitine reduces total fat mass, increases total muscular mass, and facilitates an increased capacity for physical and cognitive activity by reducing fatigue and improving cognitive functions.”(5)

In a recent study involving 12 institutionalized patients with moderate-to-late stage Alzheimer’s disease, supplementation with a vitamin/nutriceutical supplement containing folate, vitamin B6, alpha-tocopherol, S-adenosyl methionine [SAMe], N-acetylcysteine, and acetyl-L-carnitine, was found to significantly delay the decline in Dementia Rating Scale and clock-drawing text, as compared to subjects who received a placebo. According to institutional caregivers, those patients who received the nutriceutical supplementation were found to have a 30% improvement in the Neuropsychiatric Inventory and maintenance of performance in the Alzheimer’s Disease Cooperative Study-Activities of Daily Living. The authors conclude, “This formulation holds promise for delaying the decline in cognition, mood, and daily function that accompanies the progression of Alzheimer’s disease, and may be particularly useful as a supplement for pharmacological approaches during later stages of this disorder. A larger trial is warranted.”(6)

References:
1.
2. Gropper S. et.al. Advanced Nutrition and Human Metabolism, 2005, 4th edition, pp.190, 265
3. Carnitine not allowed in Canada
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4. Evans, JD et.al. “Role of acetyl-L-carnitine in the treatment of diabetic peripheral neuropathy”, Annals of Pharmacotherapy, 2008, 42(11):1686-91 < http://www.theannals.com/cgi/content/abstract/42/11/1686 >
5. Malaguarnera, M. et. al. “L-Carnitine treatment reduces severity of physical and mental fatigue and increases cognitive functions in centenarians: a randomized and controlled clinical trial”, American Journal of Clinical Nutrition, December 2007, Vol. 86, pp. 1738-1744.
6. Remington, R. et.al. “Efficacy of a Vitamin/nutriceutical Formulation for Moderate-stage to Later-stage Alzheimer’s Disease: A Placebo-controlled Pilot Study”, American Journal of Alzheimer’s Disease and Other Dementias, Dec. 2008.

Low-Glycemic Index Diet for Diabetes

December 18th, 2008

From webmd.com

Following a diet designed to keep blood sugar from rising after meals helped diabetic people keep their disease under control in a new study published in the latest Journal of the American Medical Association.

People with type 2 diabetes who ate what is known as a low-glycemic-index diet for six months had greater blood sugar control and fewer heart disease risk factors than those who followed another eating plan.

Both diets were high in fiber and low in saturated fat, and both derived about 40% of their calories from carbohydrates.

But the low-glycemic-index diet emphasized carbohydrates that had less impact on blood sugar levels, such as beans, pasta, nuts, and certain whole grains.

“These are the basic foods that your grandparents probably ate but they are no longer staples of the American diet,” lead author David Jenkins, MD, of Toronto’s St. Michael’s Hospital and the University of Toronto, tells WebMD.

What Is a Low-Glycemic-Index Diet?
The basic premise behind the low-glycemic-index diet is that all carbs are not created equal.

Some cause big spikes in blood sugar and others have little impact on blood sugar levels.

Specifically, the glycemic index measures how much a 50-gram portion of a carbohydrate raises blood sugar levels compared to pure glucose, which has a glycemic index score of 100.

Typically, foods that score higher than 70 are considered high-glycemic-index (GI) foods; those that score 55 and under are considered low-GI foods.

Many highly refined foods, including white bread, corn flakes, and instant potatoes have high GI scores; unprocessed, high-fiber foods tend to have lower GI scores.

But it isn’t as simple as saying choose unprocessed high-fiber foods.

That’s because:

Foods such as carrots and potatoes can either be high-GI or low-GI foods, depending on several factors, including how long they are stored and how they are cooked or processed.
Pasta that is cooked al dente has a lower score than pasta that is cooked longer. Rice can range from a low of 55 to more than 100, depending on variety and cooking time. The same is true with potatoes. And the riper the fruit or vegetable, the higher the score.
Research suggests that the GI response to a given food also varies from person to person and can even vary within the same person from day to day.
Some highly processed foods like cola and even some candy bars score low. A Snicker’s bar, for example, has a GI score of about 55.
“We don’t think of cola and Snicker’s bars as health food, even though they are relatively low-glycemic-index foods,” American Diabetes Association President of Medical Science John Buse, MD, PhD, tells WebMD. “If the diets of the people in the study included a lot of unhealthy, low-glycemic-index foods, I don’t think they would have gotten the benefits they did.”

Good Carbs, Bad Carbs
The low-glycemic-index dieters in the study ate plenty of legumes, peas, lentils, nuts, barley, oatmeal, pasta, and rice that were boiled briefly. They also ate low-glycemic-index breads, including pumpernickel, rye, and breads made with quinoa and flaxseed.

The foods were also paired with an eye toward keeping the post-meal blood sugar spike low. Pasta was often served with legumes, for example.

The other group of dieters ate more traditional carbohydrates including whole-grain breads and breakfast cereals, brown rice, and potatoes with skins on.

In addition:

Both groups of dieters limited saturated fats, trans fats, and white flour.
They were told to avoid pancakes, muffins, doughnuts, white bread, bagels, rolls, cookies, cakes, popcorn, french fries, and chips.
Both groups also ate five servings of vegetables and three servings of fruit a day, but the low-GI dieters avoided tropically grown fruits like mangos, bananas, and pineapple, which tend to have higher GI scores.
The 210 study participants were all taking drugs to control their diabetes and most were overweight or obese.

At the end of six months, both groups had lost about the same amount of weight. But the low-glycemic-index dieters saw more improvement in blood sugar control and heart disease risk factors than the other dieters.

Jenkins acknowledges that the difference was modest, but he adds that the findings show that the low-glycemic-index diet can help diabetic people who are highly motivated.

“This diet is not a diet for everyone, but for the person who is motivated to keep their diabetes under control, this is a good strategy,” Jenkins says.

Nutrition educator Emmy Suhl of Boston’s Joslin Diabetes Center agrees, but she says getting most people with type 2 diabetes to stick to a low-glycemic-index diet would be difficult.

“Diabetes is epidemic and this is a low-cost approach to treating it,” she tells WebMD. “The improvement they saw (in blood sugar control) was not that great, but every little bit helps. And this had the added benefit of having some reduction in cardiac risk factors.”

Vitamin B1 may reduce risk of kidney disease

December 12th, 2008

From worldhealth.net

Recent study results suggest that taking a high-dose vitamin B1 supplement each day may help diabetics reduce their risk of kidney damage.

Diabetic nephropathy, or kidney disease, is a common complication of type 2 diabetes. An early indicator of kidney disease is microalbuminuria, where the kidney leaks albumin into the urine. Researchers set out to investigate whether supplementation with vitamin B1 would effect microalbuminuria.

Type 2 diabetics were given 300 milligrams of vitamin B1 (thiamine) each day for three months. Results showed that the vitamin supplement reduced the rate of albumin excretion by 41%. Furthermore, 35% of patients with microalbuminuria saw their urine albumin excretion return to normal after being treated with the vitamin. Thus, suggesting that treatment with high-dose vitamin B1 can reverse the onset of early diabetic kidney disease.

Rabbani N, Alam SS, Riaz S, Larkin JR, Akhtar MW, Shaf T, Thornalley PJ. High-dose thiamine therapy for patients with type 2 diabetes and microalbuminuria: a randomised, double-blind placebo-controlled pilot study. Diabetologia. Published online December 5th 2008. doi: 10.1007/s00125-008-1224-4