The Risks of “Pre-hypertension”
It often seems as if treatment guidelines change every year. The levels at which experts recommend treating cholesterol, glucose levels and blood pressure have all changed recently. Some cynics say that it’s all a device by drug companies to get more people on treatment, but that’s not really true. The guidelines change as we get more evidence that not treating something leads to bad consequences in the future. A good example would be the level at which experts recommend treating elevated blood glucose. The recommendation was changed when it was discovered that even small elevations of glucose could have a dramatic impact on the development of coronary artery disease.
We now have another change, this time with blood pressure. Everyone knows that high blood pressure can be dangerous. But researchers have recently defined something that we call pre-hypertension (a systolic blood pressure 120 to 139 mm Hg or diastolic blood pressure 80 to 89 mm Hg). What was not known for sure was what impact pre-hypertension would have on the incidence of cardiovascular disease.
A study published in the journal Hypertension has clarified the issue. The research involved 2629 people participating in the twelve-year-long Strong Heart Study. Pre-hypertension was more common in people with diabetes. And as expected, from the link between blood pressure and insulin resistance, impaired glucose tolerance or impaired fasting glucose in pre-hypertensive people greatly increased the risk of developing cardiovascular disease risk. We now need to do more research to see if interventions, such as drug treatment for blood pressure control for pre-hypertensive individuals are warranted. This is particularly important if people also have impaired fasting glucose, impaired glucose tolerance, or diabetes is warranted, because risk factors for coronary artery disease are cumulative: the more risk factors, the bigger the risk.
What this means is that your health care provider should help you keep your blood pressure lower than we thought, particularly if you have a personal or a family history of problems with blood glucose or of heart disease.
Technorati tags:Hypertension Insulin resistance Diabetes mellitus Coronary artery disease
Insulin Resistance, Insulin Resistance Syndrome and Race
I often hear clinicians say that they are not too clear about the differences between insulin resistance and insulin resistance syndrome. Let me define them, and then tell you why they are so important, and why everyone needs to be informed about them.
First, insulin is a hormone produced primarily in the cells of the Islets of Langerhans in the pancreas. It has over 500 functions in the human body, but its main actions are on the regulation of the metabolism of carbohydrates and fats. Insulin enables glucose – one of the major sources of energy – to move into many of the cells in the body. Insulin is also involved in the conversion of glucose to glycogen. These two actions lower the blood glucose level.
Insulin resistance is defined as an impaired biological response to insulin. It is a condition in which many of the cells of the body – mainly in the liver, fat and muscle – become resistant to the effects of insulin. The normal responses to a given amount of insulin are reduced. As a result, higher levels of insulin are needed in order for insulin to have its effects. There are many potential causes of insulin resistance: genetic; an increase in intra-abdominal fat; smoking cigarettes; being of low birth weight; and there are some prescription medicines that can cause insulin resistance. Insulin resistance is one of the underlying causes of type 2 (maturity onset) diabetes mellitus, as well as an array of other illnesses including polycystic ovarian syndrome. Most studies have suggested that around a third of people living in the United States and Western Europe have insulin resistance, and there are marked ethnic differences.
The insulin resistance syndrome has several other names: Metabolic syndrome; (Metabolic) Syndrome X; Dysmetabolic syndrome; Reaven’s syndrome; multiple metabolic syndrome. There are several sets of criteria for defining the insulin resistance syndrome. In the USA it is usually defined as the presence of 3 or more of the following:
1. Abdominal obesity (Waist circumference >40 inches in men; >35 inches in women
2. Glucose intolerance (fasting glucose ≥110 mg/dL)
3. Elevated blood pressure ≥130/85 mmHg
4. Triglycerides >150 mg/dL
5. Low HDL (Men: <40 mg/dL; women: <50 mg/dL)
There is a constant debate in the medical literature about whether insulin resistance syndrome is an illness, and what should be included in it. It is important, because it appears to predict the development of diabetes and coronary artery disease, and between 20 and 25% of the population of the Western world has it. So what normally happens is that a person develops insulin resistance, which eventually evolves into the insulin resistance syndrome, before diabetes and heart disease appears. There can be as long as twelve years between the development of insulin resistance, and the diagnosis of diabetes, and we have very good evidence that lifestyle changes can dramatically reduce the risk of moving from insulin resistance to the insulin resistance syndrome and diabetes.
It has become quite well-known that people of African and Asian Indian heritage are at increased risk of developing insulin resistance, and some of the sequelae of insulin resistance: insulin resistance syndrome, diabetes mellitus, hypertension and gout. These may in turn lead to increased rates of myocardial infarction and strokes. A study presented last Monday at ENDO 2006, the annual meeting of the Endocrine Society in Boston helps further clarify some of these ethnic differences. Researchers analyzed data from the Insulin Resistance Atherosclerosis Study (IRAS), designed to assess relationships between insulin resistance and cardiovascular disease in a large multi-ethnic population.
The investigators divided data from female IRAS participants into different groups based on body mass index (BMI), a measure of body fat based on height and weight. A BMI of less than 25 is usually considered "normal." The analysis revealed that 47 percent of black women of normal weight had insulin resistance, compared to less than 20 percent of the Hispanic or White women. Both insulin resistance and the likelihood of developing type 2 diabetes increase as obesity increases. It had long been suspected that there was an independent effect of race, but this study not only shows that race alone may influence insulin resistance, but that we may therefore need to change the definition of obesity in women of African heritage.
The news reports on this important finding failed to mention that previous research has found something very similar in Asians from India, China and Japan. Each of these ethnic groups may develop insulin resistance, insulin resistance syndrome and diabetes without being obese, though obesity dramatically increases their risks of running into trouble.
It is relatively simple and inexpensive to measure insulin resistance, and many metabolic experts, including your humble reporter, have, for more than a decade, been measuring it in high-risk individuals. Clearly we cannot do anything much about an ethnic or genetic risk, but we can alter the way in which the body responds to that risk. If a person is insulin resistant, diet, exercise, specific nutritional and herbal interventions and occasionally medications, may all reduce the risk of developing diabetes and heart disease.
Technorati tags:Insulin Insulin resistance Insulin resistance syndrome Metabolic syndrome Diabetes mellitus Obesity Hypertension Racial differences
A Breakthrough in the Pharmacological Treatment of Diabetic Retinopathy
One of the most distressing complication of diabetes is damage to the retina of the eyes. It is more likely to occur in people with poor metabolic control, but no diabetes sufferers seem to be totally immune from it. But there is no question, that in contrast to some diabetic complications, the level of blood glucose is closely related to the risk of getting retinopathy.In people of working age living in the Western world, diabetes is the number one cause of blindness, and blindness is twenty times more common in people with diabetes than in those without it.
It is such a major problem, that I had the privilege of spending several years working on the problem at the Royal Postgraduate Medical School in London, and diabetic retinopathy was a key part of my doctoral dissertation.
So if something new turns up, I always prick up my ears.
Well, we do seem to have something new. The trouble has been that there are complex mechanisms underlying the effects of diabetes on causing complications like retinopathy. At the American Diabetes Association’s 66th Annual Scientific Sessions in Washington, DC Eli Lilly announced on June 11th, that a study headed by Aaron Vinik of The Strelitz Diabetes Institute at the Eastern Virginia Medical School, in Norfolk, Virginia of a new medicine called ruboxistaurin, almost halved the rate of the development of diabetic retinopathy over a two year period. This is astonishing, though it is important to point out that the medicine did not abolish the problem, and it was funded by the manufacturer. The medicine works by a completely new mechanism. In people with diabetes, high levels of glucose are one of the triggers of a cascade of chemical reactions in the cells of the retina, that turn on a chemical messenger called protein kinase C-β.
Though this is only a first study, and the medicine does not help with diabetic neuropathy, this is a very promising finding. Not least because most of us have failed to achieve much benefit from unorthodox medicine. I have colleagues who tell me that they have helped people with retinopathy with homeopathy and different kinds of electrical stimulation, but I’m just not sure how good those other treatments are. My guess is that if they were really effective, that independent research foundations would be falling over themselves to do research on them. But I could be convinced otherwise!
Ruboxistaurin, added to psychological, social, subtle and spiritual approaches is already looking like a very promising option for preventing problems.
Technorati tags: Diabetes mellitus Diabetic retinopathy Protein kinase C ruboxistaurin Integrated medicine
Sleep, Weight, Insulin Resistance and Diabetes
I am often asked why there seem to be such close links between food and mood. Not just comfort eating, or the sudden shock of lots of carbs when we need an energy jolt, but why drugs that alter mood so often alter appetite?
You will probably not know this, gentle reader, but I only learned of it from reading scholarly papers. Apparently many people report that using marijuana makes them very hungry. On the other hand, cocaine and amphetamine affect not just the metabolism, but also appetite. The link has to do with the evolutionary development of feeding behaviors with the motivation to find food and to be satisfied by it.
Another link that has interested me for many years is the connection between metabolism and sleep. We have always presumed that this link has to do with hibernation: even humans have maintained some hibernation responses.
There is extremely good evidence that there is an inverse relationship between the number of hours that you sleep and an increase in your weight. There have been a great many studies on this, but one of the best was published by a group of researchers from the Mood and Anxiety Disorders Program, at the National Institute of Mental Health, the Psychiatric University Hospital, Zurich, Switzerland; University of Pittsburgh School of Medicine and the Department of Psychosocial Medicine, Zürich University Hospital, Switzerland in the Journal Sleep in 2004.
A report from the BBC concerning a study presented to the American Thoracic Society International Conference in San Diego provides yet more evidence of this link between sleep and weight. Researchers from Case Western Reserve University in Ohio, followed nearly 70,000 women for 16 years. They found that women who slept five or fewer hours a night were a third more likely to put on at least 33lbs (15kg) than sound sleepers during that time. It also found that compared with women who slept for seven hours a night. lighter sleepers were 15% more likely to become obese (have a Body Mass Index (BMI) of 30 or more. {BMI is calculated by dividing your weight in kilograms by the square of your height in meters}).
Previous studies, some of which I have reported before, have shown that after just a few days of sleep restriction, the hormones that control appetite cause people to become hungrier. However the women in the study appeared to eat less. I say “appeared to,” since the use of personal evaluations of food intake are notoriously inaccurate.
In dozens of countries arond the world, I am regarded as an authority in the fields of endocrinology, metabolism and nutrition. But when a group of us tried to estimate our daily intake and compare it with meticulous diaries, we discovered that we – a group of internationally renowned experts – were off by around 500 calories per day.
All kinds of explanations have been advanced, from people who didn’t sleep getting up and binge eating; to the effects of sleep-deprived people craving high carbohydrate, high fat food; to insomnia being a result of anxiety or depression that releases hormones that cause us to lay down fat in our tummies.
For all kinds of complex biochemical reasons, I have always felt that a lack of sleep would lead to an increase in insulin resistance, that may cause an increase in the deposition of fat in key regions of the body.
Some new research suggests that I may have been right on this one. A group based at Yale University School of Medicine, in New Haven, Connecticut has just published a report that should be of interest to all of us, and in particular you multi-tasking insomniacs out there.
The investigators studied a cohort of men from the Massachusetts Male Aging Study who did not have diabetes at baseline (1987–1989) and who were followed until 2004 to look for the development of diabetes mellitus. They came to the conclusion that BOTH very short and extra long sleep durations increase the risk of developing diabetes, independent of confounding factors.
The take home message?
If you do not get 7-8 hours sleep each night, you are vulnerable to a great many problems, and perhaps the biggest of all is the risk of weight gain, insulin resistance and diabetes mellitus.
I do not recommend using sleeping tablets unless absolutely necessary, and then for just a few days at a time. Instead follow all the sleep strategies that I have talked about in earlier blog entries.
During a recent visit to Danville, Virginia, I was delighted to learn that one of the non-pharmacological approaches that I have found helpful – putting a cold compress on the abdomen – was used by General Stonewall Jackson who used this very technique that I had to learn by going all the way to China.
The bottom line? Before your sleep gets disrupted by being overweight and you develop sleep apnea, try some simple sleep hygiene, and a few of these novel techniques.
Technorati tags: Insulin Insulin resistance Insulin resistance syndrome insomnia alternative medicine resilience
Calcium, Vitamin D, Diabetes and Schizophrenia
There are some odd puzzles in medicine. For more than 100 years it has been known that diabetes is more common in people suffering from schizophrenia, bipolar disorder and probably also depression. There has also been data indicating that some children with ADD and autism have metabolic disturbances that may underlie some of the cognitive difficulties. It has also been observed in Europe that dark skinned immigrants – whose skin coloring makes them less able to make Vitamin D – are more likely to develop diabetes. Some dark skinned immigrants are also far more likely to develop schizophrenia compared with their families that stayed in sunny tropical regions. Children – particularly boys – who are breastfed and/or have Vitamin D supplements in the first year of life are less likely to develop schizophrenia in later life. Vitamin D is not only involved in calcium absorption, but also in maintaining the integrity of cell membranes. So the link between diabetes and schizophrenia may have something to do with Vitamin D.
A new study just published in the journal Diabetes Care indicates that women with high intakes of vitamin D and calcium appear to have a lower risk of developing type 2 (maturity onset) diabetes. The study from Tufts-New England Medical Center looked at data on 83,779 women enrolled in the Nurses’ Health Study. The women had no history of diabetes, cardiovascular disease or cancer when they enrolled in the study. Vitamin D and calcium intake from foods and from supplements were evaluated every 2 to 4 years. Over the 20 years of follow-up a total of 4843 new cases of diabetes were discovered. The lowest risk of diabetes was observed among women with the highest combined intakes of calcium and vitamin D compared with those with the lowest.
These are important findings, because interventions to raise both vitamin D and calcium intake and quick, cheap and easy, and may significantly reduce the risk of developing type 2 diabetes.
So how much should we take? Although we should be able to make enough of our own Vitamin D by spending even ten minutes in the sun, not everyone can do that, the sun is not without its risks, and the mechanisms for making Vitamin D become less effective as we become older. Though a balanced diet should also help provide some vitamin D and enough calcium, the data indicates that we should take in at least 1200mg of calcium each day, and 400 International Units (10 micrograms) Vitamin D each day. It is possible, though uncommon for people to take too much Vitamin D, and that can have all manner of health consequences.
Technorati tags: vitamins, diabetes, schizophrenia, calcium, Vitamin D,
A Rainy Day Question
“Millions long for immortality who do not know what to do on a rainy Sunday afternoon.”—Susan Ertz (a.k.a. J.R. McCrindle, Anglo-American Novelist, 1894-1985)
It is widely known in the scientific community that there has been a great deal of progress on aging research, much of it done behind the closed doors of pharmaceutical companies. According to Professor Tuljapurkar between 2010 and 2030, the modal, or most common, age of death will increase by 20 years if anti-aging therapies come into widespread use. This projected increase is based on some sophisticated modeling, and reflects a life-span growth rate that is five times faster than the current rate. If accurate, this would increase the modal age of death in industrialized countries such as the United States from roughly 80 years to 100.
So back to the question: if you suddenly discovered that you were going to have an extra thirty years of healthy life, what would you do with it?
I really do suggest that you start thinking about that. Assuming that you have enough money to live a decent life, what would you do with that extra twenty years? Would you:
1. Enjoy spending more time with younger members of the family?
2. Learn some new skills?
3. Make new friends?
4. Travel?
5. Read those books you always meant to?
6. Become more involved in spiritual pursuits?
7. Find a new way of serving others?
8. Sit in front of the television?
What plans or aspirations do you have that you want to add to this list?
But then I have another question for you: if your answers included any of the points from 1-7, why not do them right now? What exactly is stopping you from doing all those things today?
The Four Percent Solution
In this week’s edition of the Journal of the American Medical Association, is a study of 11,701 American over the age of 50, who participated in a national health survey in 1998 funded by the National Institute on Aging. The researchers analyzed participants’ outcomes during a four- year follow-up and examined the health characteristics that seemed to predict death within four years.
These were the questions that were asked, and this is a bit like golf: you want to have the lowest score possible. Zero would be best. The score is supposed to tell you your chance of dying within the next four years.
1. Age: 60-64 years old = 1 point; 65-69 = 2 points; 70-74 = 3 points; 75-79 = 4 points; 80-84 = 5 points; 85 and older = 7 points.
2. Male or Female: Male = 2 points.
3. Body-Mass Index: Less than 25 (normal weight or less) = 1 point. (BMI = weight in pounds divided by height in inches squared, multiplied by 703.)
4. Diabetes: 2 points.
5. Cancer (excluding minor skin cancers): 2 points.
6. Chronic lung disease that limits activities or requires oxygen use at home: 2 points.
7. Congestive heart failure: 2 points.
8. Cigarette smoking in the past week: 2 points.
9. Difficulty bathing/showering because of a health or memory problem: 2 points.
10. Difficulty managing money, paying bills, keeping track of expenses because of a health or memory problem: 2 points.
11. Difficulty walking several blocks because of a health problem: 2 points.
12. Difficulty pushing or pulling large objects like a living room chair because of a health problem: 1 point.
Score:
- 0 to 5 points = less than a 4 percent risk of dying;
- 6-9 points = 15 percent risk;
- 10-13 points = 42 percent risk;
- 14 or more points = 64 percent risk.
So what should we make of this?
The first thing is that the study is just looking at the physical aspect of life. It asks nothing about diet or family history. It also says nothing about psychological and spiritual factors that can buttress health and well-being.
So what should it mean if somebody gets a high score? Does it mean that they should expect the end and stop reading long novels? Absolutely not! A high score should be a very good indicator that you should have a talk with your health care provider and get to work on all the reversible factors on the list. And as I have pointed out before, a positive psychological outlook and regular spiritual practice have been shown to extend the length and quality of your life.
It is not given to us to know the length of our lives and plenty of people live on and on despite breaking all the rules while others die young despite a lifetime of temperance. I had an aunt who smoked heavily throughout her adult life, yet lived to be well over ninety, while one of my former students died of lung cancer in his thirties, having never smoked a single cigarette.
Genes and lifestyle are important in determining our life span, but so are the quality and integrity of our relationships, our own sense of meaning and purpose, the clarity of the subtle systems of the body and our spirituality.
So use this study not as a death sentence, but as a wake-up call.
Technorati tags: health quiz, aging, longevity
