Advanced Mediterranean Diet

I have good news and bad news.  Which would you like first?

The good news is that cancer death rates in the U.S. have dropped over the last 15 years.  The reduction is 18% for men and 10% for women.

The bad news is that the American Cancer Society projects 565,650 deaths from cancer in 2008.  If we look at deaths of people under 85, cancer kills more people than heart disease.

In men, 25% of all invasive cancers will be prostate cancer.  In women, breast cancer is the leader, comprising 26% of all cancers.  [Common skin cancers are rarely invasive or fatal and are not included in these statistics.  Melanoma, on the other hand, is invasive.]

The lifetime probability of an individual developing invasive cancer in the U.S. is about 4 in 10 (40%).  A little higher in men (45%), a little lower in women (38%).

Obesity is associated with higher risk for kidney and esophageal cancer in both sexes, prostate and colo-rectal cancer in men, and uterine, gallbladder, cervical, ovarian and breast cancer in women.  Excess body fat causes  14 to 20% of all cancer-related deaths in the U.S.  It’s reasonable to believe that reducing excess body fat will lower the risk of developing these cancers.

The traditional Mediterranean diet is associated with less risk of prostate, breast, colon, and uterus cancer.  And lower rates of cardiovascular disease.  Combine a Mediterranean diet with loss of excess body fat, and what’s not to love?

Steve Parker, M.D., author of The Advanced Mediterranean Diet: Lose Weight, Feel Better, Live Longer    www.AdvancedMediterraneanDiet.com

Reference:  Jemal, Ahmedin, et al.  Cancer Statistics, 2008.  CA Cancer Journal for Clinicians, 58 (2008): 71-96. 

Some of my casual readers may have misconceptions as to the definition of the traditional Mediterranean diet.  I use the word “diet” here not as a weight-loss program, but “the usual food and drink of a person or animal.”  Twenty-one countries have a coastline of the Mediterranean sea, and additional countries are in the Mediterranean region.  “Traditional” refers to the mid-20th century.  Observational studies around that time associated the Mediterranean diet with longer life spans, reduced rates of chronic disease (less cardiovascular disease and dementia), and fewer cancers of the colon, breast, prostate, and uterus.  There is no monolithic, immutable, traditional Mediterranean diet.  But there are similarities among many of the regional countries that tend to unite them, gastronomically speaking.  Greece and southern Italy are particularly influential in this context.

So here are the characteristcs of the traditional, healthy Mediterranean diet:

• It maximizes natural whole foods and minimizes highly processed ones
• Small amounts of red meat
• Less than four eggs per week
• Low to moderate amounts of poultry and fish
• Daily fresh fruit
• Seasonal locally grown foods with minimal processing
• Concentrated sugars only a few times per week
• Wine in low to moderate amounts, and usually taken at mealtimes
• Milk products (mainly cheese and yogurt) in low to moderate amounts
• Olive oil as the predominant fat
• Abundance of foods from plants: vegetables, fruits, beans, potatoes, nuts, seeds, breads and other whole grain products
• Naturally low in saturated fat, trans fats, and cholesterol
• Naturally high in fiber, phytonutrients, vitamins (e.g., folate), antioxidants, and minerals (especially when compared with concentrated, refined starches and sugars in a modern Western diet)
• Naturally high in monounsaturated and polyunsaturated fats, particularly as a replacement for saturated fats

Be aware that the documented health benefits may be related to a physically active lifestyle and other social and cultural issues.  For example, traditional Mediterranean mealtimes were leisurely family affairs, not a MacDonald’s Happy Meal eaten off your lap on your drive home from work.

Steve Parker, M.D., author of The Advanced Mediterranean Diet: Lose Weight, Feel Better, Live Longer   www.AdvancedMediterraneanDiet.com

Reference:  Oldways Preservation Trust

In my last blog post, I discussed the potential benefits of judicious alcohol consumption on longevity, coronary artery disease, and dementia.

I have no intention of overselling the benefits of alcohol. If you are considering habitual alcohol as a food, be aware that the health benefits are still somewhat debatable. Consumption of three or more alcoholic drinks per day is clearly associated with a higher risk of breast cancer in women. Even one or two drinks daily may slightly increase the risk. Folic acid supplementation might mitigate the risk. If you are a woman and breast cancer runs in your family, strongly consider abstinence. Be cautious if there are alcoholics in your family; you may have inherited the pre-disposition. If you take any medications or have chronic medical conditions, check with your personal physician first.

For those drinking above light to moderate levels, alcohol is clearly perilous. Higher dosages can cause hypertension, liver disease, heart failure, certain cancers, and other medical problems. And psychosocial problems. And legal problems. And death. Heavy drinkers have higher rates of violent and accidental death. Alcoholism is often fatal. You should not drink alcohol if you:
■  have a history of alcohol abuse
or alcoholism
■  have liver or pancreas disease
■  are pregnant or trying to become
pregnant
■  may have the need to operate
dangerous equipment or machinery,
such as an automobile, while under
the influence of alcohol
■  have a demonstrated inability to
limit yourself to acceptable
intake levels
■  have personal prohibitions due
to religious, ethical, or other
reasons.

Steve Parker, M.D., author of The Advanced Mediterranean Diet: Lose Weight, Feel Better, Live Longer   www.AdvancedMediterraneanDiet.com

References: Lieber, Charles S.  Alcohol and health: A drink a day won’t keep the doctor away.  Cleveland Clinic Journal of Medicine, 70 (2003): 945-953.

For centuries, the healthier populations in the Mediterranean region have enjoyed wine in light to moderate amounts, usually with meals. Epidemiologic studies there and in other parts of the world have associated reasonable alcohol consumption with prolonged lifespan, reduced coronary artery disease, diminished Alzheimer’s and other dementias, and possibly fewer strokes. Alcohol tends to increase HDL cholesterol, have an antiplatelet effect, and may reduce C-reactive protein, a marker of arterial inflammation. These effects would tend to reduce cardiovascular disease. Wine taken with meals provides antioxidant phytochemicals (polyphenols, procyanidins) which may protect against atherosclerosis and some cancers.

What’s a “reasonable” amount of alcohol? An old medical school joke is that a “heavy drinker” is anyone who drinks more than the doctor does. Light to moderate alcohol consumption is generally considered to be one or fewer drinks per day for a woman, two or fewer drinks per day for a man. One drink is 5 ounces of wine, 12 ounces of beer, or 1.5 ounces of 80 proof distilled spirits (e.g., vodka, whiskey, gin). The optimal health-promoting type of alcohol is unclear. I tend to favor wine, a time-honored component of the Mediterranean diet. Red wine in particular is a rich source of resveratrol, which is thought to be a major contributor to the cardioprotective benefits associated with light to moderate alcohol consumption. Grape juice may be just as good—it’s too soon to tell.

Don’t miss my next blogging topic - “Potential Adverse Effects of Alcohol.”

Steve Parker, M.D., author of The Advanced Mediterranean Diet: Lose Weight, Feel Better, Live Longer   www.AdvancedMediterraneanDiet.com

References:

Standridge, John B., et al.  Alcohol consumption: An overview of benefits and risks.  Southern Medical Journal, 97 (2004): 664-672.

Luchsinger, Jose A., et al.  Alcohol intake and risk of dementia.  Journal of the American Geriatrics Society, 52 (2004): 540-546.

Have you been frustrated trying to figure out what your weight is really doing when it’s up  2 pounds one day, down 1.5 the next, up 1 pound the next, then down 2.5 pounds the next?  These are normal, expected daily weight fluctuations.  Menstruating women in the week before their period may gain 5 or 6 pounds, to be lost almost as quickly as it appeared.

Google offers a helpful widget, the Google 15 Weight Tracker, that provides a moving average to tell you if you remain on track to your weight loss goal or not.  It smooths out the daily fluctuations.  To use it, you add the widget (they call it a module) to your Google Homepage, enter your goal weight, then enter your current weight periodically.  The module graphs out each data point - your weights - and calculates a moving average line.  If you are trying to lose weight, get in the habit of weighing daily, first thing in the morning after you void, in your usual sleeping clothes or underwear.

Click the link above to see how it looks and learn how to get started.

Steve Parker, M.D., author of The Advanced Mediterranean Diet: Lose Weight, Feel Better, Live Longer   www.AdvancedMediterraneanDiet.com

An up-and-coming theory to explain type 2 diabetes suggests that abnormal lipid metabolism, not glucose/sugar metabolism, is the primary metabolic defect.  Roger H. Unger, M.D., writes about this in the March 12, 2008, issue of the Journal of the American Medical Association.

Early in the writing of this blog entry, I realized it is much too technical for most of my readers.  If you are not interested in physiology, you can quit reading now.  This may be the most boring blog of mine you have ever read.  I’m writing this to solidify my own understanding of a new theory.

I assure you my prose in The Advanced Mediterranean Diet is not nearly this technical.

Still with me?  We start with definitions and physiology.  Diabetes is defined by high blood glucose (sugar) levels.  The lipid family includes triglycerides (fats and oils), sterols (e.g., cholesterol), and phospholipids (e.g., lecithin, a major cell membrane component).  Fats are almost entirely composed of trigylcerides.  When fats are broken down, fatty acids are produced.  On the other hand, fatty acids can be joined together, along with glycerol, to form triglycerides.  Glycogen is a storage form of glucose in liver and muscle tissue.  Insulin is a protein hormone produced by pancreatic beta cells.  Insulin 1) lowers blood glucose levels by driving glucose into cells, 2) inhibits breakdown of glycogen into glucose, 3) inhibits formation of new glucose molecules by the body, 4) stimulates glycogen formation 5) promotes storage of triglycerides in fat cells (i.e., lipogenesis, fat accumulation), 6) promotes formation of fatty acids (triglyceride building blocks) by the liver, 7) inhibits breakdown of stored triglycerides, and 9) supports protein synthesis.  Fatty acids in muscle tissue block the uptake of glucose from the bloodstream by muscle cells.  Fatty acids in liver tissue impair the ability of insulin to suppress breakdown of glycogen into glucose, and impairs the ability of insulin to suppress production of new glucose molecules.  In other words, an “excessive fatty acid” environment in liver and muscle tissue promotes elevated glucose levels.

Got that?  [This is very difficult material.]  Now on to the lipocentric theory of type 2 diabetes.

Type 2 diabetes may be caused by:

1. Eating too many calories, leading to…
2. High insulin levels, leading to…
3. Stimulation of fat production, leading to…
4. Increased body fat, leading to…
5. Deposition of lipids in cells where they don’t belong (that is, not in fat cells), leading to…
6. Resistance to insulin’s effects on glucose metabolism, leading to…
7. Lipid accumulation in pancreatic beta cells, damaging them, leading to…
8. Elevated blood glucose levels, i.e., diabetes.

Perhaps the key to understanding this is to know that “insulin resistance” refers to insulin having less ability to suppress glucose production by the liver, or less ability of various tissues to soak up circulating glucose.  Insulin resistance thereby leads to elevated glucose levels.  But insulin’s effect of “producing fats” (lipogenesis) continues unabated.  Excessive fats, actually fatty acids, accumulate not only in fat cells, but also in liver cells, muscle cells, pancreatic beta cells, and others.  This lipid overload can damage those cells.

If this theory is correct, so what?

Steps #1 and 2 of the lipocentric theory involve excessive caloric intake and high circulating insulin levels, leading to problems down the road.  So overweight people should restrict calories and try to lose at least a modest amount of weight.  Particularly if already having type 2 diabetes or prone to it.

And what about people with type 2 diabetes who have insulin resistance and have poorly controlled glucose levels?  Most of these have high insulin levels already, contributing to a fat-producing state.  Adding more insulin, by injection, would not seem to make much sense.  The extra insulin would bring glucose levels down, but might also cause lipid overload with associated cellular damage.  Effective clinical strategies according to Dr. Unger would include 1) caloric restriction, which helps reduce weight, high insulin levels, and fat production, and 2) if #1 fails, add anti-diabetic drugs that reduce caloric intake (exenatide?), that reduce lipid overload (which drug?), or that do both.  Dr. Unger suggests consideration of bariatric surgery, for caloric restriction and cure of diabetes.

Compared with dietary fats and proteins, carbohydrates generally cause higher circulating insulin levels.  And type 2 diabetics taking insulin shots need higher doses for higher intakes of carbohydrate. So it makes sense to me to consider preferential reduction of carbohydrate intake if someone is going to reduce caloric intake.

Dr. Unger and I agree that reduction of excessive food intake and excess body fat is critically important for overweight people with type 2 diabetes.

Steve Parker, M.D., author of The Advanced Mediterranean Diet: Lose Weight, Feel Better, Live Longer     www.AdvancedMediterraneanDiet.com

References: Unger, Robert H.  Reinventing Type 2 Diabetes: Pathogenesis, Treatment, and Prevention.  Journal of the American Medical Association, 299 (2008): 1185-1187.

I live near Scottsdale, Arizona.  The residents of Scottsdale have a reputation as being more image-conscious than the average U.S. citizen.  Think breast implants, blonde hair dye, face-lifts, Jimmy Choo shoes.  I am seeing increasing advertisements for lipodissolve, also called mesotherapy, aimed at reduction of localized fat deposits.  As a weight-loss expert, I figured I better learn more about it.  Does it work?  Are there adverse effects?  Is it just a scam to separate fools from their money?

Mesotherapy involves injection of substances into the fat tissue under the skin, leading to dissolution of that fat deposit.  It apparently kills fat cells.  The technical term would be chemical lipolysis: dead fat cells break down.  The body eliminates the residue.  Mesotherapy has been available in Europe for awhile.

I found a recently published study by physicians who are familiar with this treatment, conducted in Italy.  Study participants were 40 women, aged 20 to 55.  Average body mass index was around 21-22, right in the middle of the healthy BMI range.  They were not overweight but apparently wanted to reduce fat deposits on their thighs.  The authors described “bilateral gynoid lipodystrophy.” In less genteel terms,  these women had saddlebags.

The goal of the study was to compare two different mesotherapy chemical treatments: 1) phosphatidylcholine/sodium deoxycholate, and 2) sodium deoxycholate alone.  Injection #1 is sold in Europe as “Lipostabil.” Each woman served as her own “control:” one upper thigh was injected with #1, the other thigh with #2.  The area of treatment was limited to 80 square centimetes per side.  Think of a square 3.5 inches or 9 cm per side.  (The area injected was not actually square; more likely an oval.)  There were about 80 injections per side, about 1 cm apart.  Four treatments like this were performed every 8 weeks.

Any side effects?  The injections were quite painful, but usually short-lived.  Stinging and burning sensation lasted for some hours after injecion in all women.  Also quite common were bruising, redness, swelling, and transient nodules under the skin.  Nausea/malaise occurred in 11%, and diarrhea/steatorrhea in 16%.  Chemical #2 caused more side effects and they were slower to clear up.  Despite these side effects, the authors deemed the treatments “completely safe in the short term.”

Did it work?

Yes.  Thirty-four of the 40 women showed overall reduction of local fat.  Three of the women (8%) had no improvement at all.  Average upper thigh circumference decreased by about 4 cm (1.5 inches), from 58.48 cm down to 54.70 cm.  Loss of fat tissue was confirmed with ultrasound.  There was no difference between the two different injections.  The authors considered this a moderate amount of localized fat loss.

A commentary was made at the end of the article by a physician who performs liposuction, Naomi Lawrence, M.D.:

…it is good study, but will mesotherapy replace liposuction?  It is difficult to support the contention that this procedure has less morbidity than tumescent liposuction.  It involves four sessions, spaced 8 weeks apart requiring 80 painful injections.  It is limited to an 80 square centimeter area.  The treated subcutis becomes erythematous, bruised, and pruritic and then develops tender nodules that last about 1 month.  The mean decrease in thigh circumference is modest, approximately 4 cm on average.  Call me a pessimist but I do not think I will retire my machine or cannulas just yet.

Also, not mentioned in the article is the duration of the modest effect.  It may not be permanent.

Steve Parker, M.D., author of The Advanced Mediterranean Diet: Lose Weight, Feel Better, Live Longer   www.AdvancedMediterraneanDiet.com

References:

Salti, G., et al.  Phosphatidylcholine and Sodium Deoxycholate in the Treatment of Localized Fat: A Double-Blind, Randomized Study.  Dermatologic Surgery, 34 (2008): 60-66.

Rittes, P.G.  The use of phosphatidylcholine for correction of localized fat deposits.  Aesthetic Plastic Surgery, 27 (2003): 315-8.  [I did not read this but you may want to.  -SP]

Rotunda, A.M. and Kolodney, M.S.  Mesotherapy and phosphatidylcholine: historical classification and review.  Dermatologic Surgery, 32 (2006): 465-80.  [I did not read this but you may want to.  -SP]

Researchers at a major university in Italy today announced the successful splice of an anti-obesity gene in to the mitochondrial DNA of a morbidly obese man.

The study’s 57-year-old subject, revealed only as “Luigi”, had tried and failed numerous weight-loss programs, including bariatric surgery.  He weighed 194 kilograms (427 pounds).  Stricken with heart failure and uncontrollable diabetes and hypertension, his doctors had given him only 6 months to live.  When researchers approached him with their highly experimental and risky idea a year ago, Luigi said, “What have I got to lose?”  Scientists had heretofore demonstrated the efficacy of their treatment only in mice.

The scientists injected the “skinny gene” into their human guinea pig a year ago.  The weight literally melted away effortlessly.  Luigi lost weight down to 72 kilograms (160 pounds) and stabilized there.  He eats whatever and as much as he wants.  “I feel like a 16-year-old again!  I’ve got a new lease on life!”

Lead investigator, Giovanni Panatella, Ph.D, explained that the human mitochondria generate all the energy needed to fuel our body’s metabolic processes.  Speaking through an interpreter, Dr. Panatella said, “The foreign gene we inserted into Luigi’s genetic code disinhibits the enzyme that acts as a governor on the energy-producing NADP-ATPase pathway in the mitochondria.  Obviously, Luigi couldn’t help but lose weight.  We ‘rev’d up his metabolism,’ in layman’s terms.”

Before his pioneering work in Italy, Dr. Panatella did advanced post-graduate studies in molecular biology at the University of California - Berkeley.

Surprisingly, the source of the spliced gene is from the insect, Carausius morosus, commonly known in the United States as a walking stick.  Why this unlikely source of a “skinny gene”?  The study’s chief co-investigator, Dr. Cristobal Donatella Colon, explained: “Think about it.  Have you ever seen a fat walking stick? Think some more… NOBODY has ever seen a fat walking stick.  It’s genetically impossible.”

Through painstaking work over years, the Italian team was able to isolate and replicate the “skinny” gene.  Colleagues at T-Gen, the Translational Genomics Institute in Phoenix, Arizona, worked with the Italians to insert the gene into Luigi’s DNA.

Panatella said that large-scale, multinational, phase-3 clinical studies begin next month, and results will be presented to various scientific conferences and regulatory bodies 6 months later.  In the United States, the Food and Drug Administration has long been criticized for the expense and length of time required to bring a new therapy to the marketplace.  Political pressure has been mounting to streamline the process.  Un-named sources at the FDA expect the new treatment will sail through the myriad oversight and peer-review committees.  Regulators are well aware of the huge burden of morbidity and mortality attributable to the epidemic of obesity.

The Italians and T-Gen are in preliminary negotiations with Wall-Mart to market the gene therapy through in-store pharmacies.  The gene is delivered with a simple intravenous injection taking only a few minutes.  Researchers expect only one injection will be needed.  Wall-Mart executives are not yet prepared to say if the “skinny gene” will be available on their popular $4 prescription program.

Dr. Walter Wilett, renowned nutrition researcher and head of Harvard University’s School of Pubic Health remarked, “This is the breakthrough the scientific community has been waiting decades for.  Dr. Panatella, can you say ‘Nobel Prize in Medicine.’?”  International prestige associated with the breakthrough is expected to swell the ranks of students and researchers at the University of Bologna, where Drs. Panatella and Colon are based.

News of the astounding scientific advance reached Wall Street early today.  Stock prices of NutriSysem, Jenny Craigg, and Weight Watcher dropped precipitously, 60% on average.  Analysts are dubious about long-term viablility of the companies.

A crestfallen Marie Osmund, who recently inked a multi-year, multi-million dollar contract as a NutriSysem spokesperson, asked, “What am I gonna do now?  I’ve already spent the money!”

Cornelia Atkins, widow of diet guru and best-selling author Robert G. Atkins, said, “If you’d like 800,000 paperback books, I’ll make you a sweet deal.  They make great fire-starters for your fireplace!”

Ima Goodfellow, spokesperson for The Center for Sciences in the Public Interest, was the only wet blanket.  “I’ve got some excess weight I’d like to lose, but I’m not so sure I want insect DNA injected into me.”

Stephen Parker, M.D., author of The Advanced Mediteranean Diet: Lose Weight, Feel Better, Last Longer    AdvancedMediteraneanDiet.com

References:

Panatella, G. and Colon, C.  Effects of Enzymatic Dis-Inhibition on NADP-ATPase Energy Generation by C. morosus gene locus br459 in the human mitochondrion.   International Journal of Hermuenetics and Genomics, 56 (2008): 266-281.

Happy April Fool’s Day!