Fat, Fat, Fat

Fat, I am.

Why? One reason is I eat & drink the wrong things - I can't eat too much of anything since I had banded gastroplasty and have about a 4 bite limit on solids, less on lean meats. The limit is higher on liquids, but not infinite. So, most of my weight is probably under my control. But what about that part that is due to inheritance? My mother, and my grandmothers on both sides were obese.

There's plenty of evidence that genetics plays a role in obesity. I thought I'd gather some links here to show how varied and scattered that evidence is, as well as how ineffective current "treatments" are.

CORRELATION OF OBESITY TO THINGS UNRELATED TO BEING AN OVEREATING COUCH POTATO

FTO

Obesity gene may alter brain DNA- certain variants of a gene called FTO is linked with a 70% increased risk of obesity.

New Insight Into The Link Between Genetics And Obesity- "While genetic defects causing human obesity had been previously described, the FTO discovery was of considerable interest because the genetic variant in FTO that predisposes to obesity is very common."

PYY

Brain 'hunger pathways' pinpointed- a hormone called PYY is released by the gut in porportion to how many calories are consumed. In an fMRI study using intravenous PYY, showed that it not only lit up the hypothalamus - the main hub for controlling metabolism - but also increased activity in areas of the brain associated with reward and pleasure. Maybe food isn't addictive, but could eating be?

LEPTIN

Some of us really are addicted to food- It is suggested that the hormone, leptin, suppresses appetite by dampening our perception of how appetising certain foods are. Tests show that individuals with a very rare leptin deficiency showed increased activity in the nucleus accumbens, a brain region thought to spur drug addiction. It's speculated that obese individuals whose bodies do produce sufficient leptin have somehow become insensitive to the hormone.

Obesity-related Hormone is Higher in Children With Down Syndrome- I'm lucky to just be fat and addicted to food, if leptin resistence is part of my problem.

MELANOCORTIN

Brain clue could provide anti-obesity drugs- "Matthias Tschöp of the University of Cincinnati in Ohio used drugs that either stimulated or blocked receptors for the hormone melanocortin on hypothalamus cells in the brains of rats. Those given stimulatory drugs burned more of the carbohydrates in food, while those given inhibitory drugs converted them to fat and made extra fat in their liver. ...The same system may exist in humans, he believes, because people with faulty melanocortin receptors are often morbidly obese."

Fat Fish Put Obesity On The Hook- "The genetic change blocks the activity of a receptor, the melanocortin-4 receptor, which is at the heart of a "device" in our brains called the "adipostat." The adipostat regulates body weight homeostatically, like the thermostat in a house, and works to keep long-term energy stores--a.k.a. body fat--constant. The adipostat is what makes it difficult for people to lose weight and keep it off."

TPPII

Enzyme Promotes Fat Formation- Previously linked to making people feel hungry, the enzyme TPPII has been found to stimulate the formation of fat cells.

RENIN

Mice Lacking Enzyme Renin Stay Lean On High-fat Diet, With Little Exercise- "...mice lacking the enzyme known as renin are lean and resistant to gaining weight on a high-fat diet, even though they continue to eat just as much and don't exercise more." Maybe this should be under treatments, or possible treatments.


LIVER ENZYMES, CD36, CPT1A AND ACYL-COENZYME A DEHYDROGENASE

Metabolic Defect In Liver Can Lead To Obesity- "...intrinsic deficit in fat oxidation was associated with a decrease in the capacity to make two liver enzymes. One, CD36, is responsible for transferring fat fuels into liver cells, while the second enzyme, acyl-coenzyme A dehydrogenase, begins the oxidation process in mitochondria. When fed a high-fat diet, the obesity-prone rats overate and became obese, gaining 36% more weight than resistant animals. Fat oxidation was further compromised due to a decreased ability to make CPT1A, the liver enzyme responsible for transporting fat into mitochondria."

ESTROGEN

Obesity Risks Increase After Menopause- "As women are more at risk for being overweight or obese than men, and women are at risk for gaining weight as they age, postmenopausal women are a particularly vulnerable population."

Estrogen Curbs Appetite In Same Way As The Hormone Leptin- "Estrogen regulates the brain's energy metabolism in the same way as the hormone leptin, leading the way to a viable approach to tackling obesity in people resistant to leptin." I thought estrogen supplements had proven dangerous? Was I wrong? Maybe this article should be under "treatments" anyway.

HUMAN ADENOVIRUS-36 and SMAM-1

Common Virus May Contribute To Obesity In Some People- "In laboratory experiments they (scientists) showed that infection with human adenovirus-36 (Ad-36), long recognized as a cause of respiratory and eye infections in humans, transforms adult stem cells obtained from fat tissue into fat cells. Stem cells not exposed to the virus, in contrast, were unchanged."

Viral Infections May Be Linked To Obesity- "Dr. Atkinson reports that one study tested 52 obese humans for antibodies to SMAM-1. About 20 percent had SMAM-1 antibodies, indicating exposure to this virus. The study participants who had these antibodies were heavier and had a higher body mass index compared with the antibody-negative group."

SH2B1

Mind Over Matter SH2B1 In The Brain Regulates Obesity- "SH2B1 is expressed in many tissues related to obesity, including the brain, liver, pancreas, and fat tissue. Replacing SH2B1 in only the brain of mice lacking SH2B1 prevented the mice from becoming obese. It also prevented the mice from developing obesity after being fed a high-fat diet, indicating that SH2B1 in the brain is required to regulate body weight and fat content."

OSTEOPONTIN

When Does Being Obese Not Lead To Diabetes? When Mice Lack Osteopontin- A protein necessary for immune responses also linked to obesity and the development of insulin resistance and Type II diabetes.

SNP

Genetics Has Key Role In Obesity- "The metabolic rates of 200 obese Pima individuals were measured and revealed that two of the three known SNPs influence metabolic efficiency."

TREATMENTS

SURGERY

Stomach stapling really can save lives- It can also make your life miserable. A 29% lower risk of death from obesity-related illness, but an increase in deaths due to suicide? Is that because those who underwent the surgery lost only 14% to 25% of their body weight? A 5'7" 275 lbs. person losing 25% at 206 lbs. would have a BMI of 32.3. That doesn't really sound like success to me.

UPDATE on bariatric surgery - Was this really proof that bariatric surgeries save lives?
Sandy Szwarc evaluates the above study. Wow, what a mess.

DIETING

Obesity And The Central Nervous System- "...Dr. Levin suggested that the physiological processes which drive all of us to seek and ingest food and limit energy expenditure during periods of negative energy balance provide an irresistible drive to regain lost adipose stores in weight-reduced obese individuals. This provides a potential basis for the well-recognized difficulty of maintaining weight loss."

DIET PILLS

Three Long-term Diet Pills Show Poor Performance, Study Suggests- "The study, which looked at the long-term effectiveness of anti-obesity medications, found that three drugs recommended for long-term use - orlistat, sibutramine and rimonabant, reduced weight by less than 5kg (11 pounds). This equated to a loss of less than 5% of total body weight."

EDUCATION

Diet Education Had No Long Term Impact On Childhood Obesity- "An education programme which successfully cut the level of obesity in children by teaching them about healthy eating and discouraging fizzy drinks was no longer effective three years after the intervention came to an end, according to a study published on the British Medical Journal website."