Metabolism.com received this message from one of our readers. Her story seems typical of the sort of dilemma so many people face today. The best advice usually comes from others who face the same problem. It would be helpful to hear what others would do in her situation.
I was diagnosed with Grave’s Disease in 2009, I had RAI in 2011, after my daughter turned 3 months. Being pregnant with Severe Grave’s was the scariest thing in my life at the time. I gained weight prior to my pregnancy, during, and after RAI. My family doctor told me no matter how much you ate while severe Hyperthyroid you should have been anorexic, so something else is wrong. Continue reading
by Gary Pepper, M.D. and Andrew Levine, Pre-med
If you ask the average person to define diabetes, a typical response might be “it’s when you have unhealthy eating habits and an overabundance of sugar in your blood.” Although that is not far from the truth, a more accurate definition is that diabetes is a disorder in the way our body uses insulin to process digested food for energy and storage. A good part of what we eat is broken down into glucose, the principle form of sugar in the blood. Diabetes occurs when there is not enough insulin to push the glucose into our cells. This deprives the body of the energy it needs because glucose is metabolized as fuel by all the organs in the body. Therefore in diabetes despite an elevated amount of sugar in the blood, the cells are actually starving for energy. We sometimes conceive of glucose in the blood as the enemy , but without it we would die. Continue reading
Understanding of the various ways vitamin D effects the body is growing rapidly. Originally this vitamin was thought to only effect calcium in the blood and bone but recent research shows it possesses important influences on the immune system and cancer development. A study just published in Journal of Endocrinology and Metabolism June 2012 now shows that this same vitamin can possibly influence metabolism. A common disorder of metabolism known as Syndrome X or the Metabolic Syndrome is characterized by high triglycerides and low good cholesterol (HDL), abdominal obesity, along with elevated blood pressure and blood sugar. The researchers discovered those with vitamin D levels between 16 and 20 were 75% more likely to develop the Metabolic Syndrome within 5 years than those with vitamin D levels above 34 (levels below 30 are considered low).
Whether low vitamin D is the cause of the Metabolic Syndrome is unclear. Vitamin D prevents fat cells from reproducing, helps the natural process of triglyceride breakdown and helps regulate blood sugar by making insulin work more efficiently. Without enough vitamin D the fat cells could multiply faster, triglyceride levels accumulate and blood sugar rise as is seen in Metabolic Syndrome.
As I have explained in previous posts at metabolism.com, vitamin D is also related to development of hardening of the arteries (atherosclerosis) and obesity in Type 2 Diabetes which could be considered a more advanced form of Metabolic Syndrome.
Doctors’ efforts to monitor vitamin D levels are being hindered by new regulations by Medicare and private insurance carriers to deny payment for vitamin D screening. Lately, a number of my patients’ vitamin D tests were denied by insurance carriers with patients being charged over $200 per test because it was not “indicated”.
Recommendations for vitamin D supplementation are debated. When skin is exposed to sunlight it manufactures vitamin D so there is thought that people who get sun exposure should not need vitamin D supplement but that is not borne out in reality. Previously the recommended daily allowance (RDA) was 400 units per day an amount which has been increased slightly for the elderly. Some experts recommend 1000 unit daily or more. In my practice I generally recommend starting at 1000 units and then rechecking 25 hydroxy vitamin D levels a few months later. Some individuals require 4000 unit or more daily to achieve vitamin D levels over 30. When purchasing vitamin D the D3 form appears to be converted in the body more rapidly than the D2 variety. High priced brands of vitamin D, in my opinion, are a waste of money.
Gary Pepper, M.D.
The old saying, “The way to a man’s heart is through his stomach” implies there is a deep connection between emotions and eating. My guess is no one is really surprised by this idea. Both men and woman can identify ways in which their mood and appetite are intertwined and it is no mere quirk of man’s personality that this is true.
Evolution tells us that we were born to eat. The earliest creatures in the world’s history were simple eating machines. Their bodies consisted of an entrance for food, a digestive tract and an exit for refuse. In order to become more efficient at getting food creatures developed a system to locate food and to move toward it. This system is known as a nervous system. The first creature to have this ability is the worm. Eventually the nervous system controlling the digestive system (enteric nervous system) began to sprout nodes which were early brains. As time went on and the brain became better developed it split off from the nervous system that controlled the digestive tract. Everything that followed in evolution, has served the purpose of developing increasingly efficient brains (central nervous system) for acquiring the fuel of life.
Another example of how deeply connected the gut and brain are, is to look at the development of the fetus. When a human fetus is still just a lump of jelly, the digestive and nervous systems are one structure. Soon this organ splits into two, one to become our gastrointestinal tract and the other the brain and spinal cord (central nervous system). Even though they become physically separated the chemical signals used by the gut and nervous system remain virtually identical. These chemicals comprise the groups known as neurotransmitters and hormones.
The same chemicals in the digestive tract that cause the intestines to twist and convulse (peristalsis), in the brain stimulate the emotion of anxiety. This explains why people get “butterflies” in the stomach or diarrhea when they are nervous. The brain chemicals involved in depression can cause constipation. The syndrome of irritable bowel disease (IBS) with its cycles of diarrhea and constipation is thought to be a reflection of an emotional rollercoaster. The chemical relationship between mood and appetite is even more complex but no less real. One of the most common side effect of mood altering drugs is increased appetite and weight gain. Just ask anyone who has been on an anti-depressant drug such as Prozac, Zoloft or Abilify. The chemical in marihuana that gets people high is famous for triggering the eating binge called “the munchies”.
Appetite suppressant drugs often have effects on mood and can be the source of major side effects. One new generation of appetite suppressants being developed, Acomplia, failed to be approved by the FDA because it caused severe depression and suicidal thinking.
In the next part of this series we will look at ways we can influence the brain to control our appetite.
Puberty occurs when areas within the brain awaken beginning a cascade of hormone signals which conclude with the gonads (ovaries and testicles) increasing their production of the female and male sex hormones estrogen and testosterone. Under the influence of these hormones a child begins the transition from childhood to sexual maturity. In boys puberty is associated with a growth spurt, the appearance of facial, axillary (arm pit) and pubic hair, acne, deepening of the voice, growth of the testicles and penis while girls undergo a growth spurt, develop breasts, acne, pubic and axillary hair, and growth of the clitoris.
Historical data shows the average age of puberty today is many years sooner than in previous generations. Most experts attribute earlier puberty to better nutrition. A recent article in metabolism.com reviewed how “over-nutrition” accelerates obese children into puberty sooner (referred to as precocious puberty) than normal weight children. The latest studies on causes of precocious puberty suggests that a child’s social environment also exerts an important influence on the timing of puberty. Researchers in Madrid publishing in The Journal of Clinical Endocrinology and Metabolism 95:4305 2010 analyzed the age of puberty in normal children, adopted children and children whose families immigrated (children not adopted but subject to high levels of personal stress) to Spain. Adopted children were 25 times more likely than other groups of children to undergo precocious puberty (breast development before the age of 8 years in girls, and boys under 9 years of age with testicular growth). Over-all girls were 11 times more likely than boys to demonstrate precocious puberty.
Researchers speculate that socio-emotional stresses early in life of children who are later adopted result in changes in the brain that cause premature maturation of vital nerve pathways. This early brain maturation later results in stimulation of the pituitary gland, turning on the hormone pathways that cause puberty. This seems strange to me because various forms of deprivation in childhood can also delay puberty. For example, girls who have anorexia remain child-like in their body development and may fail to menstruate even into their late teens. A decade ago I studied hormone levels in adults during the stress of illness and surgery and found this lowered the sex hormone levels in their blood. This makes sense from an evolutionary point of view because during stressful conditions nature wisely cuts off the reproductive hormones. Why make babies if the environment is hostile in some way? Why the opposite occurs in children under stress of adoption is an interesting but unanswered question.
Gary Pepper, M.D.,
As a culture we don’t plan for a sudden halt in scientific advancements. Our tendency is to expect progress to be rapid and continuous. My prediction is that in certain areas of medical science we are likely to see not only a halt in progress but a slipping backward. In particular, the realm of medical weight management is in complete disarray at this time. Two new drugs designed to induce weight loss have been shot down by the FDA in the last few months. The first is Qnexa, developed by Vivus Inc. Interestingly, Qnexa combines two drugs already approved for use in the U.S. One of the drugs is phentermine which is a medication used for decades as an appetite suppressant. The other is a common drug used to treat seizures with the brand name Topamax (topiramate) which also induces weight loss. The drug performed admirably in clinical trials with most participants losing over 10% of body mass. The FDA cited excessive risks of the drug in its statement of rejection. One wonders why the drugs are still being marketed separately if they are so dangerous.
The latest drug to be rejected by the FDA is Lorgess (lorcaserin), developed by Arena Pharmaceuticals. This drug, not as effective as Qnexa, produced 5% body mass loss in about half of participants in clinical trials. Lab animals showed a tendency to develop breast tumors when exposed to the medication, adding to the FDA’s decision to reject the drug application based on safety concerns.
I am a strong advocate of drug safety and regulation. On the other hand we know obesity, and with it Type 2 diabetes, is epidemic in the U.S. I regard weight loss as the “holy grail” when treating type 2 diabetes and yet it is the most difficult goal to achieve. Any drug which could assist in weight loss is highly desirable in the treatment of Type 2 diabetes. Not only does blood sugar improve with weight loss but also blood pressure and cholesterol readings show declines. All three of these parameters are known to be prime contributors to the main cause of death in diabetics, cardiovascular disease.
It has already been 10 years since the last drug was approved specifically for a weight loss indication. The failure of these two latest medications to achieve approval is certain to cause the pharmaceutical industry to severely curtail if not abandon further investment in this type of drug development.
Why is the FDA so reluctant to approve a weight loss pill? This is a complex issue but requires an answer. A new weight loss inducing medication is certain to be highly anticipated and widely prescribed. Therefore, from the very first day of approval the FDA must take responsibility for the well being of millions of people who are likely to take the medication. We are a society which demands our medications deliver miraculous cures with no side-effects. If someone perceives they have been injured by a medication our legal system is primed to unleash brutal retribution on everyone remotely involved in the approval process. Abuse and injury with a medication designed to cause weight loss is almost a certainty. This is a no-win situation for the administration of the FDA.
I predict it will be at least another 10 years before a medication for weight loss is approved by the FDA. Unless there is a change in the climate of litigation in this country it will take longer than that. In the meantime the only new developments in weight loss drugs will be the result of exploiting appetite suppressant effects which are the “side-effect” of medications approved for other purposes.
Gary Pepper, M.D.
It seems obvious that cutting away part of the stomach and intestine should cause weight loss. With a smaller stomach and less intestine fewer calories can be absorbed per day causing weight loss. Surgeons who perform gastric by-pass were puzzled however, by how fast their patients showed metabolic improvement after undergoing this procedure. They noticed many of their diabetic patients could be taken off diabetic medication immediately after surgery before weight had been lost. Scientists looking into this phenomena discovered unsuspected ways gastric by-pass improved metabolism.
The intestines produce hormones which regulate blood sugar and appetite. GLP-1 is among the best known of these intestinal hormones. GLP-1 is the basis of a whole new generation of medications used to treat diabetes such as Byetta, Victoza, Januvia and Onglyza. GLP-1 lowers blood sugar, stimulates the pancreas and reduces appetite. After gastric by-pass increased amounts of GLP-1 are produced by the remaining intestine. In a study published in the Journal of Clinical Endocrinology and Metabolism (95:4072-4076, 2010), researchers at St. Luke’s Hospital in New York discovered that levels of oxyntomodulin, another intestinal hormone that suppresses appetite and acts like GLP-1 on blood sugar levels, is doubled after gastric by-pass.
These exciting discoveries help explain why obese diabetics can often be sent home without any medication to control blood sugar immediately after undergoing gastric by-pass surgery. Although most insurance plans do not cover gastric by-pass surgery, dramatic improvements in patients after the procedure with greatly reduced medication costs may convince insurance companies that paying for the procedure will result in better outcomes and save them money in the long run.
Gary Pepper, M.D.
Due to the potential for abuse and high cost, growth hormone treatment in adults is the subject of much controversy. I believe that treating adults with growth hormone deficiency is many times an appropriate and beneficial choice. Firming up my conviction for treating adult growth hormone deficiency is a recent study conducted in the Netherlands and UK published in the Journal of Endocrinology and Metabolism (JCEM 95:3664-3674, 2010). The researchers compared Body Mass Index (BMI), waist circumference, triglycerides, and HDL (good cholesterol), between normal adults and those with low growth hormone levels due to deficient pituitary function (hypopituitarism). All measurements of obesity and lipid metabolism were significantly worse in the young adults (younger than 57 years) with growth hormone deficiency compared to normal adults of a similar age.
As I pointed out in previous articles at metabolism.com, growth hormone levels naturally decline as we get older. The authors of the present study note that growth hormone levels decline 14% per decade in adults. I conceive of this as one of the ways nature gets rid of us after we complete our biological/reproductive functions, since without growth hormone our muscles, immune and nervous systems, decline, leading to death. It’s planned obsolescence… what is typically referred to as aging. In the recent study senior citizens have equivalent levels of obesity and abnormal lipid metabolism as young adults with growth hormone deficiency. The authors note the effect on the body of growth hormone deficiency in young adults is equivalent to 40 years of aging. The theory that growth hormone functions to preserve our tissues during youth and aging results from its absence, appears confirmed by these results.
Most normal young adults aren’t growth hormone deficient and the population that would qualify for growth hormone treatment from this group is small. What about older adults with low growth hormone who are troubled by the “natural” decline in their body function? Should or could we treat this much larger population with growth hormone? It is my experience that private and federal insurers will not pay for this treatment regarded as “cosmetic”. On the other hand, there will be physicians who will comply with a request for growth hormone treatment from individuals who possess enough cash and motivation. Less affluent or determined individuals will have to contend with natural aging just as our ancestors have done for thousands of years.
This information is for educational purposes only and is not intended as medical advice or treatment.
Gary Pepper, M.D.
What comes to mind when considering the term “inflammation”? A festering pimple, or perhaps a high fever, an infected tooth, toe, abscess? These are typical examples of inflammation. Inflammation may exist in many other forms however, including possibly obesity.
Inflammation describes the immune system when it is activated. The presence of pus or fever are obvious forms of this. More subtle forms of inflammation can exist in the body. Recently, researchers from Australia, presented evidence that obesity itself is associated with abnormal activation of the immune system, or in other words, inflammation. This inflammation might in turn, cause type 2 diabetes. It is already becoming clear that the inflammation associated with obesity contributes to insulin resistance, the first step in the development of type 2 diabetes. In a study just published in the June volume of the Journal of Clinical Endocrinology and Metabolism (95:2845-2850, 2010), patients with either type 2 diabetes or pre-diabetes were evaluated for the distribution of inflammatory blood cells before and after gastric band surgery. Abnormal immune activation or inflammation was detected in this group. After an average of 13% weight loss following gastric surgery, the scientists found up to an 80% reduction in inflammatory blood cells. Many of the patients were able to significantly reduce their diabetic medications after the weight loss. The conclusion is that inflammation may result from obesity and is reversible when significant weight is lost. Metabolic problems like diabetes improve as the inflammation is reduced, as well. Therefore, inflammation may be part of the reason people develop diabetes as their weight increases.
Studies like this will provide new avenues for attacking the development of type 2 diabetes due to excessive weight gain, and possibly to help find ways of combating obesity, as well.
Gary Pepper, M.D.
Type 2 diabetics are more prone to heart attacks, peripheral vascular disease and stroke. All of these can be linked to hardening of the arteries (atherosclerosis). Known risk factors for atherosclerosis are high cholesterol levels, obesity and high blood pressure. A recent study now demonstrates that atherosclerosis and obesity are associated with low vitamin D 25 levels in African-American type 2 diabetics. This study published in the March issue of JCEM was conducted at Wake Forest University School of Medicine. The researchers found that low vitamin D levels in diabetics are more common with increasing obesity and also with greater degrees of atherosclerosis of the aorta and carotid arteries (which supply the brain with blood).
Whether low levels of vitamin D cause any of these diseases or are simply another abnormality found in people with these illnesses has yet to be determined. Future studies are being planned in which obese type 2 diabetics are treated with vitamin D to see if these diseases can be improved.
Gary Pepper, M.D. Editor-in-Chief, Metabolism.com