Type 1 Diabetes Definition. The definition of type 1 diabetes is a state of absolute deficiency of insulin. In this scenario, the pancreas is unable to produce sufficient insulin to maintain proper glucose homeostasis in the body. As a result, individuals with type 1 diabetes must rely on insulin taken by injection to stay alive.

Why Does the Pancreas Fail? The exact cause of type 1 diabetes is not known for certain but the available evidence suggests that some type of autoimmune reaction is generally involved. This results in damage to the islet cells that produce insulin, and eventually cause failure of insulin production.

Is there a cure? One way to treat the disease is to have a pancreas transplant. This is a procedure where a whole pancreas is donated from a brain-dead organ donor and transplanted into a person requiring the pancreas. Someone who is living is not able to donate a whole or part of a pancreas as we each have a single pancreas that is required for our survival. A pancreas transplant is a major operation and requires that the individual stay in the hospital for a week or more and be on anti-rejection drug therapy for the rest of their life. Once a person receives a new pancreas that is functioning normally, they are no longer considered diabetic and no longer need to take insulin. Their blood glucose levels are regulated by the islet cells in their new transplanted pancreas.

More Recently. A new procedure has evolved that shows some promise as an alternative to a whole pancreas transplant. This procedure involves the isolation of islet cells from a donated pancreas and the transfer of those cells through a blood vessel to the liver where the cells will live and produce insulin in the recipient’s body. Although these individuals must also be on anti-rejection therapy there are several advantages to this procedure. These advantages include a less invasive procedure, a lower cost, and a much shorter hospital stay.

The Islet Cell Transplant Procedure. There are several steps in the islet transplant procedure that will be outlined as follows:

• The Donor. The islet cells used for the procedure are obtained from a brain-dead donor.
• Before the Transplant. The process prior to transplantation includes an assessment by the transplant physicians with a physical examination, eye examination, and blood work.
• The Transplant. The Transplant. The transplant is performed by a radiologist in the hospital. A catheter is placed in a vein in the abdomen. Islet cells are injected into the vein and end up in the liver where they will live. This procedure is performed using a local anesthetic in the skin of the abdomen, similar to the anesthetic in a dentist’s office. It is otherwise painless.
• After the Transplant. Recipients of a transplant will be seeing the transplant physicians and team on a regular basis after the transplant. They will be taking medications to keep the islet cells functioning and free of rejection. The exact medications used are currently being studied and are changing and improving with time and research.

How many transplants are required? From previous research, it appears that most people will require more than one islet transplant for successful treatment. Some people have required up to three transplants.

Risks of Transplantation. The risks associated with any transplant are infections and increased risk of developing cancers. These risks are side effects of the medications used to prevent transplant rejection. It is not clear at this point how common these risks will be in people receiving islet transplants. So far, there have been no reports of any such complications. However, this is a risk that all people who receive a transplant will be made aware of and will need to accept.

The Hypothesis for the Islet Cell Transplant Study Program. Intuitively we may assume that the islet cell transplant will definitely make a huge improvement in health and quality of life. That may not be true! Will it delay complications? What about the anti-rejection drugs? In terms of costs are the benefits to the patient really there? It may be found to be a great improvement in diabetes care, but we will not know if this in fact is true until studies are performed to look at this question.

Who is eligible for the research study? The trial population to be enrolled will include approximately 50 subjects, male and female, between 20 and 80 years of age who have Type 1 diabetes. Patients must also have some problems with their eyes and kidneys, related to diabetes, but those patients who have heart trouble or are considering pregnancy will be excluded. Patients must also reside in the greater Vancouver area.

How are patients evaluated for eligibility? Patients are evaluated by the islet transplantation physicians. Eye examination, urine tests, and blood work, will be monitored on a regular basis. Before transplantation, all patients will be treated with the best medical treatments for diabetes that we currently have which includes controlling blood sugars well with insulin injections, and treating any other medical problems such as high blood pressure or high cholesterol.

What is optimal medical therapy? Glycemic Control (blood sugars)

• Target fasting or pre-meal blood sugars by glucometer 4-7 mmol/L
• Target HbA1c <0.70 to be followed every 3 months.

These targets are based on the Diabetes Control and Complication Trial (DCCT), which demonstrated an approximately 50 percent reduction in eye, nerve, and kidney complications with intensive treatment for hyperglycemia.

Blood Pressure Control. Hypertension (blood pressure >140/90 mmHg) should be treated to attain target blood pressure <125/70 mmHg to prevent progression of renal disease.Treatment for high blood pressure is important because elevated diastolic blood pressure is a risk factor for the development of macular edema, and elevated systolic blood pressure is a risk factor for loss of vision.

Lipid Control (Blood fats). All patients will be treated to target values for the following fasting lipid profile:

• LDL-C level <2.5 mmol/L
• Total Cholesterol:HDL-C ratio <4
• Triglyceride level <2.0 mmol/L

Based on 10 year risk of coronary artery disease >30%, or a history of cardiovascular disease, or diabetes from the Recommendations for the Management and Treatment of Dyslipidemia , CMAJ, May 16, 2000; 162(10) 1441-1447.

Renal Protection (Kidneys). All patients with >300 mg/day of albumin in their urine and microalbuminuria (30-299 mg/day albumin in their urine) will receive ACE inhibitor treatment even in the absence of hypertension. Based on Should All Patients with Type 1 Diabetes Mellitus and Microalbuminuria Receive Angiotensin-Converting Enzyme Inhibitors? A Meta-Analysis of Individual Patient Data. Annals of Internal Medicine. March 2001, volume 134, pages 370-379.

Patients will be randomly selected from the group to receive an islet transplant.Of the group of 50, there will be 10 people at a time who will carry pagers so that they can be contacted in the case a transplant becomes immediately available.

Study Flow Chart

1. Meet Inclusion Criteria
2. Retinopathy Assessment
3. Cardiovascular Assessment
4. Transplantation Team Assessment
5. Exclusion Criteria and Assessment
6. Trial of Optimal Medical Therapy (3 months)
7. Collect Data on End Points on Optimal Medical Therapy
8. Await random selection for islet cell transplantation.

The Islet Cell Transplant Study (Blood fats). Despite medical treatment, complications related to diabetes still occur. This study will determine the rate of progression of complications related to type 1 diabetes in subjects with microalbuminuria and retinopathy on optimal medical therapy. The subjects will receive optimal medical treatment which includes: glycemic control, blood pressure control, lipid profile control, and all patients will be treated with an ACE inhibitor.

Trial Schedule

• Planned inclusion of first subject: started March 11, 2002
• Planned inclusion of last subject: When 50 patients have been recruited.

The study has started enrolling patients at this time. We anticipate that the first transplant will take place near the end of 2002 or early 2003.

Rationale for the Trial. These subjects will ultimately await random selection for pancreatic islet cell transplantion. The data collected in the first part of the study will ultimately be used to compare against data after islet cell transplantation.

The primary endpoints (key data measurements collected) are glycemic control, glycemia frequency, and progression of complications:

• rate of progression from microalbuminuria to proteinuria (kidney damage)
• rate of progression of diabetic non-proliferative retinopathy to proliferative retinopathy (eye damage).

The secondary endpoints of the study are:

• renal failure (elevated creatinine)
• end stage renal disease
• myocardial infarction (heart attacks).

Subjects will be randomly selected into the treatment arm or control arm. All subjects will be treated to the targets for optimal medical therapy (see previous page). Subjects in the treatment arm will randomly receive a transplant when there is a pancreas available. Randomization is similar to flipping a coin, and not controlled by the investigators. Both cohorts will be followed for primary and secondary endpoints (described earlier).

All study participants will be closely followed before the transplant as well as afterwards to determine whether the transplant has improved their quality of life as well as prevented progression of diabetes related problems.

Summary

Pancreatic islet cell transplantation is a potential new promising treatment for patients with type 1 diabetes. Currently, there are no clinical studies to show that pancreatic islet transplantation is better than the current optimal medical treatment for type 1 diabetes. There is also no long-term data on the effects of islet transplantation in the progression of complications related to diabetes. These complications include decrease in kidney function, diabetes-related eye disease, cardiovascular disease, and death. Currently, there is also no data on long-term safety of pancreatic islet transplantation. Studies to answer these questions have not yet been performed.

The study we are now starting will try to answer these questions. We will be comparing patients who receive optimal medical treatment for type 1 diabetes to patients who receive pancreatic islet cell transplantation. We hope to determine what differences in outcome and complications are seen between these two treatments. Should pancreatic islet transplantation be shown to be a superior treatment for type 1 diabetes than our current optimal medical therapy, we hope to be able to provide this treatment in improving the health of patients with type 1 diabetes.

Michelle Fung is a clinical fellow specializing in endocrinology and metabollism.

The post The Islet Cell Transplant Program appeared first on BC Diabetes Foundation.

The results of the Heart Protection Study were announced in November at the American Heart Association conference. This study was conducted in Britain and involved randomizing 20,500 volunteers, at high-risk for heart disease, to either 40 mg Zocor (a statin – one type of cholesterol lowering medication) or a placebo. They were then followed for 3-5 years and the incidence of heart attacks, strokes and re-vascularizations (procedures to open or by-pass blocked blood vessels) was assessed. There was also an additional part in the study where they randomized volunteers to a nutritional supplement containing 250 mg vitamin C, 600 IU vitamin E and 20 mg of beta carotene compared to those taking a placebo. The announcement of the results was a front page story in both the Vancouver Sun and the National Post last November. You can also find information on the study at www.hps.com.

What were they thinking?

The Zocor Arm. As a reminder Zocor is a member of the statin family of cholesterol lowering medications. It acts in the liver by inhibiting an enzyme involved in the synthesis of LDL, the ‘bad’ cholesterol. All of the statins on the market definitely work and typical LDL cholesterol reductions are in the order of 35 to 60% depending on the type and dose of statin used. LDL is believed to function as the ‘bad’ cholesterol in that it can contribute to the deposition of fat on arterials walls leading to narrowing and even blocking blood vessels. It follows therefore, that if we are able to lower the LDL cholesterol in a high-risk group of volunteers, then we should see a reduction in events such as heart attacks, strokes and revascularization procedures.

The Vitamin Arm

It is generally believed that antioxidants in the blood can reduce the activity of unstable free radicals which are thought to contribute to the progression of disease states such as heart disease and cancer. Therefore, by boosting the levels of the bloods antioxidants we would also hypothesize a reduction of events as mentioned above. With this in mind individuals were randomized to either placebo or a daily vitamin regimen of 250 mg vitamin C, 20 mg beta carotene, and 600 IU vitamin E.

The Findings In The Vitamin Arm

There was no significant effect of the vitamin intervention. While the investigators were disappointed with this result it really isn’t that surprising. They didn’t approach the vitamin arm from the same aggressive perspective that they did the statin arm. I spoke with a dietician who reviewed the doses of vitamins used and she made it clear that they did not approach the accepted safe upper limit. This was especially true for vitamin C as 250 mg daily is barely a supplemental level for most people, not a therapeutic dose. Doses of vitamin C in the 1000-2000 mg range are tolerated by most people, especially if taken as a slow release form. Given the doses for all three vitamins they used I don’t feel the protocol design allowed the vitamin supplement question to be properly addressed.

There are cardiologists and researchers in this field who feel differently. Vancouver’s Dr. Jiri Frohlich feels this study is ‘the nail in the coffin for antioxidants for people with heart disease’ and he is not alone. Many experts in this field of research feel this has once and for all answered the antioxidant question in terms of prevention of heart disease. Some of the experts do agree, however, that antioxidants started at an earlier age or in nutritionally deficient populations could theoretically provide some benefit although this has yet to be demonstrated.

The Zocor Arm Findings

The results of the Zocor arm of the study really were quite convincing. What was found was that all events including heart attacks, strokes and revascularization procedures were significantly reduced in those individuals taking Zocor compared to those individuals taking the placebo. This was found to be true regardless of age, sex, heart disease history or prior cholesterol levels. They found that risk was reduced even for people who had normal cholesterol at the start of the study.

The overwhelmingly positive results of this study are likely going to influence the prescribing habits of many physicians. This will not be a surprise given the scientific merit of this study and the strength of the conclusions. Unfortunately they may lose sight of what the study demonstrated. It showed that lower LDL and total cholesterol in a high-risk group reduced events and saved lives. We should use this information as incentive and as a catalyst for addressing the causes of elevated cholesterol and take a stronger preventative approach rather than accepting statin therapy as the first step.

Implications To Our Health Care System

Let’s consider the cost implications of putting people in BC on Zocor at 80 dollars a month. The newspaper quoted Dr. Rory Collins, the study’s lead investigator, as saying the results showed that treating 14 people for 5 years would prevent 1 heart attack/stroke/revascularization. The cost of Zocor for 14 people would be $67,200 and then we must consider the additional cost of GP visits and monitoring liver/muscle enzymes for safety purposes since not everyone tolerates statins. That’s the cost for 14 people to prevent one event. The study authors add that for every 40 individuals treated for 5 years we could save one life. The cost of saving one life therefore, would be approximately $192,000. In terms of BC let’s consider putting 100,000 Lower Mainland people (5% of 2 million) on Zocor since it estimated that about 5% of Canadian adults are on some statin and these numbers are likely to increase following the release of these study findings. That works out to almost 480 million dollars over five years to prevent an estimated 7140 events and 2500 deaths. Canada wide this could represent over 7 billion dollars. These are rough estimates but it is clear that it could represent a significant amount of our health budget and we must ask two questions. Is it worth it? Could these events and deaths have been prevented by other means?

Patents

It is true that when the patent on Zocor expires a cheaper generic form of Zocor should reduce the overall cost to the health care system. I contacted the local pharmacy to compare the cost of some of the generic statins currently available with the brand name original. The two generics available were 21% and 37% cheaper than their brand name versions and the cheapest was approximately half the cost of Zocor, the statin used in the Heart Protection Study. Be aware efficacy does vary between different statins and dosing.

The Savings

Will these expenses be offset by savings in hospitalizations and reduced burden on health care by the high risk individuals who would benefit the most from statin therapy? The care for patients with vascular disease is extremely expensive in terms of emergency visits, surgeries, rehabilitation etc and there is no doubt the savings would be substantial. Whether they would offset the costs is not known. I would suggest that a large scale cost-benefit assessment be performed before we put millions more Canadians on statins.

The New Aspirin?

Dr. Collins even went so far as to say that #39;statins are the new aspirin#39; based on their findings and the potential therapeutic applications. There are at least two major differences between aspirin and statins. Aspirin is only pennies a day and the cost is typically absorbed by the patient. Secondly, there is the safety issue and the cost associated with it. I don#39;t know any physicians who recommend blood safety tests for aspirin users. It isn’t required whereas typically a GP would arrange a blood test to check on a patient’s liver enzymes following initiation of statin treatment to make sure the patient is tolerating the medication. Referring to statins as the ‘new aspirin’ is misleading from a cost and safety perspective even though it may be true from the perspective of reduced events and deaths.

Not All Statins Are Created Equal

The study showed that Zocor does not appear to present a major safety risk based on the data in this study, the details of which were not provided. Dr. Salim Yusuf, Division of Cardiology at McMaster University, suggests that the safety profile for Zocor in this study was actually better than that for ASA. This is of course the best safety data we have yet on statins. For that reason many doctors will likely prescribe Zocor for patients just starting on a statin since safety has been demonstrated. It is not reasonable to assume that all other statins will have the same safety performance over the long term since they are all a little different. This is clear from the recent experience with cerivastatin (Baycol) which was removed from the market following a number of deaths and adverse experiences as a result of rhabdomyolysis, a potentially life-threatening condition which occurs when a large number of skeletal muscles die. Baycol may be unique in terms of some of it’s properties yet all statins present a potential danger. As the use of different statins becomes wide-spread it will be important to monitor patients who start taking them.

Our Unhealthy Heart Crisis

What was most sobering in the media articles that followed the HPS announcement was that there are so many high-risk people. Maybe some of the 7 billion dollars that may get spent on statins in Canada over the next 5 years could be spent on programs that try to address the underlying causes of the current Unhealthy Heart Crisis. The statin may do its prevention ‘thing’ regardless of lifestyle changes which is sad in a way. The statin doesn’t necessarily improve the health of any individual. What it does is reduce the risk of heart attack and stroke by 25%. We should think of good health as a sense of wellness and a high quality of life, not merely as a low-risk factor. High risk is often a function of being overweight, inactive, smoking and having a poor diet. We may have someone on a statin who is just as unhealthy as before or perhaps worse. They are simply at lower risk of heart attack and stroke and therefore represent less potential burden on the cardiovascular component of the health care system.

Could a degree of risk reduction have been accomplished by other means? I think the answer to that is yes. Lifestyle modification is one of the simplest ways to reduce your risk for the progression of heart disease and the eventual reduction of MIs and Stroke. The foundation is diet, exercise and stopping smoking. These changes lead to a major improvement in the quality of life, more energy and they empower the individual at the spiritual level giving them a sense of control over their life. One lifestyle convert is often enough to infect 10 others by example and through enthusiastic conversation. That can be a wonderful thing to witness and share in the ongoing cycle of healthy changed lives. Furthermore, if individuals do experience an MI or stroke the better fit individuals tend to have more rapid recoveries, shorter hospital stays and better long-term prognosis.

Reality

Could a lifestyle intervention arm have accomplished what this study accomplished with Zocor? With 100% compliance perhaps, but in the real world I don’t believe so as much as I would like to. The incredible amount of lowering of LDL cholesterol with statins is virtually impossible to achieve consistently with lifestyle intervention. In a group of 20,000 research volunteers compliance with pill taking is far more likely than compliance with a time consuming, energy demanding change in diet and activity. At the individual level however we can all make our own choices about changing our lives and LDL isn’t the only risk factor. Don’t let my earlier statement discourage you from making positive changes in your lifestyle because those changes will make a difference to your entire body, not just your heart disease risk profile.

Conclusions

Statins will undoubtedly play a key role in treating patients who are at high-risk for heart disease. There are people who will benefit from and who should be on statins. Given the recent findings of the Heart Protection Study there may be a trend to put a far greater number of lower-risk people on statins. If you are one of the low-risk individuals considering statins I would ask that you consider all your alternatives, and ask your doctor plenty of questions.

Eric Norman is a research scientist investigating heart disease.

The post The Benefits of Cholesterol Lowering: Reviewing the Heart Protection Study appeared first on BC Diabetes Foundation.

The Islet Cell Transplant Program is gearing up at Vancouver Hospital with the assistance of the BC Endocrine Research Foundation. The program which is described in detail in this issue will be conducted as a research study investigating whether having an islet cell transplant results in improved health/quality of life when compared to conventional non-surgical diabetes care.

The results of the large Heart Protection Study were released last fall and demonstrated the benefits of cholesterol lowering therapy using a statin. Now we should consider how this information can be incorporated into our approach to health and wellness, as an individual and as a society.

Enjoy this issue and feel free to check out our website and contact us if there is something you would like to see on the website that isn’t there.

The post From the Editor appeared first on BC Diabetes Foundation.

Dr. Diane Finegood with the Canadian Institute of Health Research spoke about having 58% prevention of diabetes with lifestyle intervention for people with high risk for type 2 diabetes. I can concur that my best HbA1c results were when I was called by a diabetes education nurse once a week as part of a research study conducted by the BC Endocrine Research Foundation. Dr. Finegood reported that even 30 minutes of exercise a day 5 days a week made an impact on the onset of diabetes and related complications. She also warned that obesity has been identified as the number 1 health problem in North America, is a major predictor of type 2 diabetes and the problem increases annually.

Dr. Jerilynn Prior, professor of endrocrinology at UBC spoke about what’s new in perimenopause. Contrary to common belief the levels of estrogen can actually be high and chaotic during perimenopause. Also, research is showing there is bone loss before menopause. Stress hormones were discussed as bad for bones and birth control pills have been shown not to build bone. Exercise, nutrition and some supplements can be helpful during perimenopause and after. Dr. Prior is involved with the Canadian Multicentre Osteoporosis Study (CAMOS).

Andrea Swan an RN from the Victoria James Bay Community Health Project spoke about what women want in midlife. Her involvement combines social, health services, community services and youth and womens education. She has identified that mid-life women have not had the opportunity to speak to their mothers about the changes during perimenopause and menopause because of cultural norms. In the year 2002 there is an overwhelming amount of information from media and professionals. In groups, such as the ones she facilitates at James Bay, she helps women find their way through the maze of information so they can make informed decisions about their health and life choices.

I found this an extremely enjoyable symposium with lots of valuable information. Many thanks to the panel and our very able host, Joyce Resin. Another success story for the BC Endocrine Research Foundation.

The post Women’s Health Symposium November 4th 2001 appeared first on BC Diabetes Foundation.

Having hot flushes? Past menopause? No risks for heart disease?

We are looking for women to participate in a 4 month research study on blood vessel function and hot flushes. The study is being run by:
Dr. Jerilynn Prior
Professor of Endocrinology,
University of British Columbia.

To participate, you must:

• Be menopausal (2 – 10 years since your last menstrual period)
• Currently experience hot flushes and/or night sweats
• Not be taking hormones (estrogen, progesterone, tamoxifen or birth control pills)
• Have no heart disease or history of heart disease
• Have no risk factors for heart disease

In this study we will be comparing the effects of raloxifene (Evista(r)) and progesterone (Prometrium(r)) on blood vessel function and hot flushes. Blood vessel function can indicate your risk for heart disease. The study will be conducted at the Echelon Centre, at W. 8th and Ash.

For more information, contact:
Christine Hitchcock, PhD
Phone: (604) 875-5917
Email: chitchco@vanhosp.bc.ca

This study is funded by Eli Lilly. Prometrium® and placebo have been donated by Schering Canada.

This study is investigator-initiated. The investigator retains the right to publish the findings of this study, regardless of the nature of the results.

The post Research Study on Blood Vessel Function and Hot Flushes appeared first on BC Diabetes Foundation.

Introduction

Women in midlife increasingly hear the words “estrogen deficiency” spoken as the ultimate in bad news. “Everyone knows” that low estrogen levels cause heart disease, osteoporosis, Alzheimer’s and frigidity. Right? But as Dr. Susan Love (renowned breast surgeon and author of Dr. Susan Love’s Hormone Book) states, “If estrogen deficiency’s a disease, all men have it!” [Love 1997]

Our purpose here first is to put women’s midlife experiences and concerns into a new and more accurate hormonal picture. Specifically, I’d like to present new information about high estrogen levels in the perimenopause. Not low, not even normal, but estrogen levels that are higher than those of the (sexiest) 20 year-old woman! Secondly, I’ll discuss how you can tell when your estrogen levels are high and out of balance with progesterone, the other important hormone for women. And finally, we’ll review the many ways a woman can help herself through perimenopause, “Estrogen’s storm season!”

What is perimenopause?

Women have often called “menopause” everything they experience during the changing times of midlife. However, now that we know about perimenopause, a hormonally distinct time in midlife, it is important to use the right names. Menopause means that a year has passed since a woman’s final period. Perimenopause refers to the long and changing time until a woman “graduates” into menopause. The newest name for perimenopause is “menopausal transition”.

The first perimenopausal change commonly masquerades as increased premenstrual symptoms (sometimes called PMS). A regularly menstruating woman may have her first migraine, start waking after two or three hours of sleep and toss and turn. Finally she may suddenly flood during what was a normal period or start having night sweats. On average the perimenopause lasts at least four and commonly eight to 10 years. The good news is that perimenopause ends! I am an expert on the perimenopause primarily because I have now graduated! I survived a rough 10-yr perimenopause and my own experiences told me that the experts had it all wrong about dropping or deficient estrogen levels!

High and swinging, not dropping estrogen levels in perimenopause!

Many studies in the last 20 years have measured estrogen levels in perimenopausal compared with premenopausal women. Each study, however reports by summarizing that estrogen levels are dropping.

Surprisingly, they don’t bother to mention the high levels they also found [Burger, Dudley, et al. 1995].

When all of the studies are put together (Figure 1, above), and the average perimenopausal estrogen levels are compared with average levels in young women, it is clear that estrogen levels are about 30% higher than normal during perimenopause [Prior 1998].

Let’s consider estrogen levels from a population-based study of over 300 Australian perimenopausal women (Burger, Dudley, et al. 1995). Each woman had a blood test 3-8 days after the start of flow-each woman’s level is a dot in Figure 2.

This shows lots of estrogen variation and high levels occurring not only in the regularly menstruating women (group 1) but also in women who were between 3 and 11 months since their last period.

Not only are most of the levels higher than the average end-of-flow estrogen levels for 20-35 year olds (dotted line) but many are even higher than the highest point at the middle of the cycle for 20-35 year olds (solid line). But what did these very good scientists say in summary? “Perimenopause is characterized by dropping estrogen . . .levels” [Burger, Dudley, et al. 1995].

The study we just discussed [Burger, Dudley, et al. 1995] also measured a strange new hormone called “inhibin”. I believe it is because inhibin, the ovary’s normal brake-type hormone, begins to slack off in its job of keeping the pituitary’s Follicle Stimulating Hormone (FSH) in line, that the perimenopausal ovary goes through its grand finale [Prior 1998]. Lower inhibin levels allow FSH to increase and to stimulate several rather than just one follicle (the nest of estrogen-producing cells surrounding an egg). As a consequence estrogen levels rise and become unpredictable [Prior 1998].

The other big hormonal change of perimenopause is that progesterone levels are too low [Prior 2001]. Progesterone, the important ovarian counterbalancing hormone to estrogen which is made after an egg is released, is produced in lower levels even when cycles are still regular [Santoro, Rosenberg, et al. 1996]. We know that normal progesterone levels are needed to prevent bone loss in young women [Prior, Vigna, et al. 1990]. We also know that too much estrogen with too little progesterone makes for heavy periods or frequent flow.

Clues that estrogen levels are high or out of balance with progesterone

There are many things you can observe that will tell you that you are experiencing the typical perimenopausal hormone imbalance-too-high estrogen and too-low progesterone levels. You’ll need to be a record-keeper and a sleuth to discover what is happening for you because such a wide array of experiences is possible. Early in the process of my perimenopause I had a disturbing dream-more like a nightmare. I woke suddenly, early one morning, from a most vivid dream that I was pregnant! I could feel my swollen and tender breasts, my moist and heavy-feeling vagina, the heat and expectation in my body. In my dream I felt like I had a belly full of a full term baby. I woke thinking that I had really lost it! At fifty, with my two children grown, the last thing in the world I wanted was to be pregnant. But after some thought, I began to understand that it was my subconscious self’s way of saying goodbye to my fertile years.

Many of the things I felt in that dream, however, are also high estrogen signs: swollen and tender (sometimes lumpy) breasts, increased vaginal mucous and a heavy pelvic feeling similar to cramps. High estrogen and progesterone levels in pregnancy are normal and necessary. In perimenopause however, estrogen levels are high but progesterone levels are not.

Heavy flow, bleeding less than 3 weeks apart, continual spotting or clotting and increased cramping are all signs that estrogen is too high. For the amount of estrogen, progesterone levels are also too low [Santoro, Rosenberg, et al. 1996]. Canadian researcher, Dr. Patricia Kaufert, who has done one of the best studies about what women experiences during perimenopause, found that women who have flooding menstruation are likely to start the time of skipped periods in perimenopause [Kaufert, Gilbert, et al. 1987].

Heavy and unpredictable flow is not only horrible to live with but they can cause iron deficiency, low blood counts (anemia) and deep fatigue. Although some women will soak a half a box of tampons a day, soaking 16 or more pads or tampons in any (entire) period is abnormal. The culprits are too much estrogen and too little progesterone or whether or not your uterine muscle has a fibroid. Fibroids disturb the endometrium (uterus lining) less than 10% of the time and are therefore, rarely the cause for abnormal flow.

What about breast swelling and tenderness in perimenopause? It is normal for the breasts to swell a bit during the week before flow. It is sometimes normal to feel tenderness in the front or nipple area of the breast at the middle of the cycle when estrogen hits its high peak. But continuously swollen breasts, front-of-the45breast soreness before flow or for more than three days each month means high estrogen levels. During perimenopause women may become forgetful. We now know that stress makes for memory problems. And the high estrogen levels of the perimenopause (added to the stress of this major life change) make cortisol and other stress levels higher (Kirschbaum, Schommer, et al. 1996). No wonder it feels like PMS-city! One nurse said it very well, “At (peri)menopause life can turn into one long pre-menstrual experience. Hormones slap you up against the doors of your unfinished business” (Kelsea 1991).

Are hot flushes (or flashes) from low estrogen?

Periods once a month tell us our estrogen levels are normal. Many doctors still believe that night sweats and hot flushes are caused by low estrogen levels. If that were true, how come so many perimenopausal women start having night sweats when their periods are perfectly regular? The answer is that hot flushes/night sweats are caused by decreases or swings in estrogen levels even if they are still high. The brain becomes used to the young normal estrogen levels and, when it has been exposed to the high levels during the perimenopause, it rebels as those levels drop, even to normal. What happens with a hot flush is similar to what a drug addict goes through during withdrawal-a major brain discharge of stress and other hormones. It is this hormonal discharge (along with the flush) that causes the anxious feelings, nausea and chest pain as well as the feeling of heat and the sweating that go with them. So if someone tells a you your flushes are in your head just tell them that “darn tootin” they are!

I first twigged that I was perimenopausal when I woke abruptly one dark November morning in 1990 feeling MAD! I looked for a cause-my dog and my partner were sleeping soundly, all was quiet in the house and in the neighborhood. But my heart was pounding, my legs wouldn’t lie still and I was ready to do battle.

Then I felt a weak and woozy wave of heat and began to sweat. A day later my period started. I had no more night sweats until the day before my next period.

I had learned an important thing-in the early years of perimenopause; night sweats are a clue that your period is coming (Figure 3) [personal communication, G. Hale, 2001].

Another new observation is that women who have increased premenstrual symptoms early in the perimenopause are more likely to have a difficult time with hot flushes at the end of perimenopause and in early menopause. That information came from the same Australian study I told you about earlier {Guthrie, Dennerstein, et al. 1996}. High estrogen levels cause premenstrual symptoms. It makes sense that the brain would react when these high levels do their chaotic dance in perimenopause or eventually settle out to the normally low levels of menopause.

What can I do to help myself through the rough times in the perimenopause?

The first and most important thing to realize about perimenopause is that, ready or not, we must go through a major life change-change in body, change in fertility, even change in concepts about ourselves [Page 1994]. A number of years ago I was captured on a National Film Board video “Is it hot in here?” saying I was only 22 times 2 and was looking forward to menopause as a normal phase of life! But, when perimenopause hit me, though my mind said I was okay with it, although I have all the children I ever wanted, and despite my fulfilling job and lots to look forward to, I went through times of real sadness. Losing youth, fertility and even predictable periods are justifiable reasons for feeling blue. It helped me and will help you to deal with this natural sadness if you talk with friends, family and perhaps even a counselor about these important and often hidden feelings. I also suggest reading a book by Vancouver counselor, Lafern Page, Menopause and Emotions: making sense of feelings when feelings make no sense [Page 1994].

The next most important thing we can do to help ourselves in perimenopause is to take time to care for ourselves. A friend and important pioneer in the work of bringing perimenopause information to BC women, retired public health nurse, Pat Chadwick, said, “The first two letters of the word menopause are ME!” That means we need to take time out for exercise, meditation and having a latte with a friend. We also may need to say “no!” to more overtime or to continuing to make our 12 year old’s lunch. Get your priorities straight-take care of yourself!

I was significantly helped in my perimenopause by keeping the Daily Perimenopause Diary ((c)1991). To allow many women access to this self-record tool we have made a video that both describes the hormonal changes of perimenopause and explains what you can learn from using the diary [Prior 1999]. A completed diary showing 8 days of flow in which you soaked 6-10 tampons a day is more likely than your complaints about it to convince your family doctor that you need a blood count and some progesterone therapy!

Our bones face at least three challenges during later perimenopause: swinging estrogen levels (causing increased bone loss), too low progesterone levels (causing less new bone to be formed) and higher stress hormone levels (causing both bone loss and less new bone) [Prior 1998]. It is therefore a good idea to increase your daily calcium intake (from food and supplements) to 1500 to 2000 mg/d (spread across the day with food and 400-600 mg at bedtime). Calcium supplementation also decreases premenstrual symptoms [Thys-Jacobs S, Starkey, et al. 1998] and will help with sleep and with restless legs that can start in perimenopause. In addition to calcium, you should also take at least one multiple vitamin to provide 400 IU of Vitamin D each day. Our skin can’t make vitamin D during October through March from the slanty northern sunshine we get in most of Canada and the northern U.S.. If you have a family member with osteoporosis (by bone density measure or a broken bone with low trauma) you probably should take 800 IU/d of Vitamin D.

Night sweats are troubling and sleep-disturbing. Vitamin E in a dose of 400 to 800 IU each day may help in addition to regular exercise (both walking and heart-rate raising aerobic exercise), decreasing stress [Swartzman, Edelberg, et al. 1990} relaxation and slow deep breathing. It may also be that eating foods made from soy such as tofu or drinking soy beverages on a regular basis will decrease hot flushes [Murkies et al., 1995].

Heavy and too frequent periods are the most urgent problem for us in perimenopause. What can we do about periods, flooding, cramps and the risk for anaemia? If you are regularly soaking over 12 pads or tampons during a whole period, I suggest you start taking iron because you are likely to have low iron stores if not anemia. Take one (inexpensive) tablet of ferrous gluconate a day (34 mg of iron, an inexpensive, green pill). This can be purchased from the drugstore without a prescription (but be sure to tell your doctor). For menstrual cramps, as well as to decrease heavy flow, ibuprofen (Advila, Motrina or generic) 200 mg, can be used at the first hint of cramps and repeated four or more times a day. Ibuprofen use has been shown to decrease the amount of blood loss. If the cramps are really bad, take two tablets at the first hint of cramps and take one more each time you start to get the heavy pelvic feeling that cramps are returning.

If taking ibuprofen and iron doesn’t resolve the perimenopausal flow problems and anemia and if bleeding lasts longer than a week or occurs at shorter than 3-week intervals, you need to see your family doctor. Ask for a prescription for progesterone (Prometrium(r) or medroxyprogesterone) which works to prevent estrogen’s over-stimulation of the endometrium.

Progesterone also controls or even stops flow depending on the dose and your estrogen levels. It is ideal to take it cycle days 14 to 27 after the first day of flow (Figure 4). If your cycles are shorter (flows less than 25 days apart), start the progesterone on day 12 and continue through day 25.

Each time you start it finish the full 14 days of progesterone. Full doses (3 capsules of progesterone =300 mg/d or 1 10-mg tablet of medroxyprogesterone) are absolutely necessary because we are trying to balance very high estrogen levels. It may be necessary to take high doses for a number of months. If you have migraine headaches, ask your doctor to prescribe it every daily because often hormone changes can trigger migraines.

In most cases of heavy/frequent flow there is no need for a referral to a gynecologist, an endometrial biopsy, a D & C or a pelvic ultrasound. Keep in close contact with your family doctor. Unless both you and your doctor decide that at least six months of full or high dose cyclic progesterone hasn’t helped don’t see a surgeon whose common “choices” are oral contraceptives, uterine lining ablation (killing the endometrium) or hysterectomy. I suggest you decline the oral contraceptives your doctor may offer because even “low dose” pills contain high estrogen that won’t suppress the estrogen your ovaries are already making in abundance! If at all possible, refuse the hysterectomy or endometrial ablation (killing the uterine lining) surgery that gynecologists often offer. Either surgery takes away flow that provides one of the few clues we have to the ovary’s mysterious antics during perimenopause and helps us to know when we are menopausal. Like the rest of perimenopause-this heavy flow will get better!

Summary

So, let’s review. We have talked about the perimenopausal puzzle of high rather than low estrogen levels and the paradox that many doctors believe estrogen treatment will help. Now you will be able to recognize when your estrogen levels are too high and will know that, although life may be miserable right now, this is likely quite normal and will pass. You can now figure out that you are perimenopausal, even though flow is regular, when you start getting night sweats and or premenstrual symptoms increase. Most importantly, when flow is abnormal and persists in being so, you can ask for cyclic full-dose progesterone treatment to help balance your high estrogen effect in the brain and bone and uterus. And, if you are taking good care of yourself and find you still can’t cope with premenstrual symptoms, waking in the wee hours of the morning and night sweats, you could ask your doctor for cyclic progesterone therapy for those reasons also.

Most important-understand that you, like me, can survive perimenopause!

As Ursula LeGuin, the science fiction writer says “The woman who is willing to make that change must become pregnant with herself, at last” [LeGuin 1991].

Jerilynn Prior is an internationally known expert on progesterone and an active researcher and educator.

References

1. Love S: Doctor Susan Love’s Hormone Book. San Francisco: Random House, New York, 1997; 1-348.
2. Burger HG, Dudley EC, Hopper JL, et al: The endocrinology of the menopausal transition: a cross-sectional study of a population-based sample. J.Clin.Endocr.Metab. 1995; 80: 3537-3545.
3. Prior JC: Perimenopause: The complex endocrinology of the menopausal transition. Endocr.Rev. 1998; 19: 397-428.
4. Prior J. C. Perimenopause– the ovary’s frustrating grand finale. A Friend Indeed 15(7), 1-4. 1998.
5. Prior JC: Ovulatory changes with perimenopause Endocrine Ageing in Women. In: Endocrine Facets of Ageing in the Human and Experimental Animal. Veldhuis JD, Laron Z, eds. London: Wiley Publishers (in press), 2001.
6. Santoro N, Rosenberg J, Adel T, Skurnick JH: Characterization of reproductive hormonal dynamics in the perimenopause. J Clin Endocrinol Metab 1996; 81:4, 1495-1501.
7. Prior JC, Vigna YM, Schechter MT, Burgess AE: Spinal bone loss an ovulatory disturbances. NEJM 1990; 323: 1221-1227.
8. Kaufert PA, Gilbert P, Tate R: Defining menopausal status: the impact of longitudinal data. Maturitas 1987; 9: 217-226.
9. Kirschbaum C, Schommer N, Federenko I, et al: Short-term estradiol treatment enhances pituitary-adrenal axis and sympathetic responses to psyhosocial stress in healthy young men. J Clin Endocrinol Metab 1996; 81: 3639-3643.
10. Kelsea M: Beyond the stethoscope: a nurse practitioner looks at menopause and midlife. In: Women of the 14th Moon: writings on menopause. Sumrall AC, Taylor D, eds. Freedom, California: The Crossing Press, 1991; 268-279.
11. Guthrie JR, Dennerstein L, Hopper JL, Burger HG: Hot flushes, menstrual status, and hormone levels in a population-based sample of midlife women. Obstetrics and Gynecology 1996; 88: 437-442.
12. Page L: Menopause and emotions: making sense of your feelings when your feelings make no sense. Vancouver: Primavera Press, 1994; 1-241.
13. Thys-Jacobs S, Starkey P, Bernstein D, Tian J, The Premenstrual Synrome Study Group: Calcium carbonate and the premenstrual syndrome: effects on premenstrual and menstrual symptoms. Am.J.Obstet.Gynecol. 1998; 179: 444-452.
14. Swartzman LC, Edelberg R, Kemmann E: Impact of stress on objectively recorded menopausal hot flushes and on flush report bias. Health Psychology 1990; 9: 529-545.
15. Murkies AL, Lombard C, Strauss BJG, Wilcox G, Burger HG, Morton MS: Dietary flour supplementation decreases post-menopausal hot flushes: effect of soy and wheat. Maturitas 1995; 21: 189-195.
16. LeGuin UK: The Space Crone. In: Women of the 14th Moon: writings on menopause. Sumrall AC, Taylor D, eds. Freedom, California: The Crossing Press, 1991; 3-6. Copyright Jerilynn C. Prior October, 2002

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Anne Fiddick, the chair of our foundation’s Public Advisory Council, has provided us with her assessment of the recent Women’s Midlife Health Symposium. I was there and found it extremely informative with great talks and excellent questions from the audience.

You’ll be glad to know we are officially launching our website this month. You’ll find more detailed information on the website in the small article on this page. Please visit the site and let us know what you think and what you would like to see on the site.

I hope the New Year is treating you well and all your resolutions are still intact.

The post From the Editor appeared first on BC Diabetes Foundation.

A satisfying meatless meal, the following is a delicious and nourishing makeover of traditional Shepherd’s Pie:
Lentil Shepherd’s Pie
(adapted from Rose Elliott’s The Supreme Vegetarian Cookbook)

• 1 cup green or brown lentils
• 2-3 tsp olive oil
• 1 large onion, finely chopped
• 1 carrot, diced
• 1 green pepper, chopped
• 2 celery stalks, chopped
• 2-3 garlic cloves, minced
• 2 teaspoons dried mixed herbs (e.g. sage, oregano, savoury, basil)
• ¼ cup tomato paste
• 2 tbsp tamari sauce
• ¼ cup vegetable stock or water
• 2-3 tbsp chopped fresh parsley (or 2 tsp dried)
• 3-4 medium boiling potatoes (idaho or russet), cooked and mashed
• 2-3 tsp milk (soy milk)

Rinse lentils thoroughly, discard any small stones or debris. Put lentils into a saucepan, cover with water and bring to a boil – turn down to medium-low and cook until tender (approx 45 minutes). Add a little more water if necessary, so lentils do not dry out. Drain. Preheat oven to 400 F.

Heat a large saucepan to medium temperature. Saute onions in olive oil until soft. Add carrots, green pepper, celery and garlic. Saute until tender (about 2 minutes). Add herbs, tomato paste, tamari sauce, cooked lentils, parsley and the soup stock or water. Add salt and pepper to taste. Turn heat to low and cover pan for 5 minutes to combine flavours.

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It is often said that you either have type 2 diabetes or you don’t. Your physician may tell you that you can’t have just a touch of diabetes or be a little bit diabetic. Why is this? The main reason is that there is a definition of diabetes based on several strict criteria and you either meet the criteria or you don’t. The criteria are as follows:

1. Fasting blood sugar > 6.9 millimoles/litre (mmol/l). Individuals are asked to refrain from eating for 12 hours prior to going to the lab to have a blood sample drawn and the sugar concentration of blood plasma determined. A normal fasting blood sugar is ~ 6.0 mmol/l.
   or
2. Fasting blood sugar between 6.1 and 6.9 mmol/l and a 2 hour post-glucose load blood sugar > 11.1. The Oral Glucose Tolerance Test (OGTT) is used to determine the latter by having individuals consume a drink containing 75 grams of pure glucose (yummm…) and then determine the blood plasma glucose concentration 2 hours later.

Health care professionals need these diagnostic criteria in order to make decisions regarding patient care. In other words the line has to be drawn somewhere. If diagnosed as diabetic you will be referred to a doctor who specializes in diabetes care and possibly education and counseling at a diabetes clinic. In the past those who didn’t meet the criteria were typically sent on their way. What is done now is individuals who almost meet the criteria are looked at more closely.

What if you almost meet the criteria?

Individuals who have a fasting blood sugar between 6.1 and 6.9 mmol/l but who have OGTT values between 7.8 and 11.0 mmol/l are referred to as having Impaired Glucose Tolerance.

They are not defined as diabetic but they have a 5% annual probability and a 35% lifetime probability of becoming diabetic. They are walking around with blood sugars higher than normal much of the time and this can effect their health. Many of these individuals are on the road to becoming diabetic.

A second group that almost meets the criteria is those who have a fasting blood sugar between 6.1 and 6.9 mmol/l but their OGTT comes back < 7.8 mmol/l. These individuals are referred to as having Impaired Fasting Glucose (or Impaired Glucose Homeostasis). Although the probability of these individuals becoming diabetic may not be as high as the Impaired Glucose Tolerant it is definitely a warning sign.

From a diagnostic perspective you either have diabetes or you don’t based on these criteria. From a physiological perspective there is a gradient from the normal individuals where glucose is well controlled to the type 2 diabetic where glucose levels are out of control. The nature of the disease is such that you don’t go from one end of the gradient to the other overnight. It is a gradual process as the body becomes more resistant to insulin and the pancreas is unable to provide adequate amounts of insulin to overcome the resistance.

How prevalent is undiagnosed diabetes and glucose intolerance?

In 1998 a group of researchers asked this very question with regards to the Canadian population (refernce). They designed a program to have family physicians screen their patients (over 40 years of age) for diabetes. The physicians were randomly selected to ensure accurate representation of the Canadian population, balancing proportions between provinces as well as between rural and urban settings and between men and women. They enrolled 9,042 patients in this study.

What did they find?

They found that 2.2% of the group they screened had diabetes and didn’t know it. Another 3.5% of the group screened had either Impaired Glucose Tolerance (0.6%), Impaired Fasting Glucose(2.5%) or were probably diabetic (0.4%, based on limited information). These numbers are close to a previous estimate (reference) that 3-5% of Canadians are walking around with undiagnosed type 2 diabetes. Hyperglycemia (high blood sugars) develops gradually and Type 2 diabetes is often only recognized 5-12 years after hyperglycemia develops. Prior to Type 2 Diabetes diagnosis prolonged hyperglycemia may have already caused some damage to target tissues (heart, eyes, kidneys, nerves). This can occur in the absence of the classic symptoms of diabetes (list). This is why early detection is essential and why screening programs for diabetes are rapidly expanding.

Equally important is the early detection of impaired glucose tolerance and impaired fasting glucose. Detecting these warning signals can permit early intervention and halt the damage caused by persistent hyperglycemia. Typically these physiological states are warning signs that your diet and exercise habits aren’t suited to your genetic make-up. They may be suited to your friend Fred down the street who eats and does exactly what you do and yet stays slim and trim; but you aren’t Fred. Genetics plays a huge role in determining our susceptibility to type 2 diabetes and the stages preceding it. The accumulating evidence suggests that there are as many as ten or more genes that may play a role in the onset of type 2 diabetes. If you are diagnosed with type 2 diabetes or any of the stages preceding it you will have to learn to modify your lifestyle in order keep your genes happy.

Is Type 2 Diabetes Preventable?

In most cases Type 2 Diabetes is a preventable disease. It has been said that type 2 diabetes is the result of a ‘clash between genes and the environment’ ( 5 ). Since we can’t change our genes, not at this point in time anyway, we need to change the environment, more specifically our diet and exercise habits. But does it really work. A Finnish research group decided to try and answer that question (6).

The Research Study. They recruited 522 middle-ages, overweight subjects with impaired glucose tolerance. This population was chosen because they have a greater probability of developing diabetes making it possible to show significant effects of the study intervention in a relatively small study population in just a few years.

Volunteers with impaired glucose tolerance were randomized to either a control group or an intervention group. The control group was given general oral and written information about diet and exercise at the start of the study and at each annual visit thereafter. There were no individualized programs offered to them.

The Intervention.The intervention group was more intensive. They were given detailed advice about how to achieve the goals of the intervention; the goals being:

• a reduction in weight of 5% or more
• total intake of fat less than 30% of energy consumed
• saturated fat less than 10% of energy consumed
• increased fibre and
• thirty minutes of exercise a day.

Nutritional advice was tailored to each subject based on food records. Volunteers in this group had 7 sessions with a nutritionist during the first year and every three months thereafter. These volunteers also received information on increasing their level of physical activity including both endurance training and strength training.

Did it make a difference?

At baseline the characteristics of both groups were identical in all respects. They observed that during the trial (mean follow-up of 3.2 years) the cumulative incidence of diabetes was 58% lower in the intervention group (63% for men and 54% for women) compared to the control. But this is conservative since not all those in the intervention group adhered to their recommendations, and for ethical reasons, the control group also received some guidance.

In the assessment they went one step further and looked at how successful the individuals were in achieving the goals of the intervention. This adherence was assessed for all 5 recommendations listed earlier. In those individuals who achieved 4 or 5 of the goals there was no one who developed diabetes after a mean of 3.2 years follow-up. Alternatively, when none of the goals were achieved, diabetes appeared in 38% and 31% of the intervention and control group, respectively. The message here being you can join as many gyms as you want and see a dietician regularly but unless you are willing to actually make the changes it’s not going to help you.

This is not the first study to demonstrate diabetes prevention with changes in lifestyle since large studies in Sweden(7) and China(8) have shown similar results. In these two studies, however, the individuals were not randomly assigned to the control and interventions groups. This recent study randomized individuals to the two groups and also ensured that the two groups were identical at the beginning of the study.Another point of interest in the Finnish study was that a weight loss of as little as 5% can make a huge difference in the incidence of diabetes. In other words the changes don’t have to be overwhelming. Setting reasonable goals and taking small steps in the right direction can pay off.

Is screening important?

Before getting screened you should consider risk factors for type 2 diabetes. Some risk factors to consider are:

• greater than 40 years of age
• central obesity
• has a parent sibling or child with diabetes
• high-risk ethnicity (Hispanic, aboriginal Canadian, Asian, African-Canadian, Pacific Islander)
• had gestational diabetes
• has given birth to a baby weighing more than 10 pounds
• if the results of your test indicate you are glucose intolerant based on any of the criteria you should take action early on.

Why wait?

You can get started right now of course without even going to your physician or a clinic and it won’t cost you or the health care system a penny. Consider what you now know to be some steps of a diabetes prevention program as outlined in this research study and think of how you can incorporate some or all of these recommendations into your life.

Why should I bother if I may not have diabetes?

The interventions used in this study to prevent diabetes are excellent recommendations for everyone. They are fundamentals of what we know to be a health promoting lifestyle. They can make you feel better, sleep better, have more energy and prevent or delay other health problems such as heart disease and osteoporosis. This is true whether or not you have any form of glucose intolerance.

In Summary

In summary the recommended changes in lifestyle should include changes in diet and exercise. More specifically I would recommend the following goals.

Dietary goals: Aim for a total fat intake of less than 30% of total energy consumed and reduce saturated fat to 10% or less. You may also want to reduce your cholesterol intake as well. Boosting your fibre intake to greater than 15 grams/1000 calories is a good idea. If you smoke then stop as soon as possible.

Exercise goals: Strive to improve cardiovascular fitness. Brisk walks, cycling, swimming, running. It doesn’t have to be one big workout. Research has shown that you still benefit from a small number of shorter activities during a day. For example, two or three 15-20 minute walks during the day if you don’t feel you have time for one big 45 minute walk. Whatever works for you. Be sure to consult your physician if you have any doubts about whether you should engage in a fitness activity.

Strength training should also be considered given our current understanding of glucose disposal and muscle mass (refer to the lead-off article?. It is also excellent for your bones. Be sure to consult an instructor if you are using weights for the first time and start slowly, gradually increasing your intensity as your strength increases and your body becomes accustomed to the activity. The combination of cardio activities and weight training should equal about 4 hours per week.

Eric Norman is a research scientist investigating heart disease in post-menopausal women and in individuals with type II diabetes.

References

1. Diabetes Screening in Canada (DIASCAN) Study. Leiter et al., June 2001. Volume 24 Number 6. Diabetes Care.
2. Tan H and DR Maclean. 1995.Epidemiology of dabetes mellitus in Canada. Clin Invest Med.. Volume 18:240-246.
3. Muggeo, M. 1998. Accelerated complications in type 2 diabetes mellitus: the need for greater awareness and earlier detection. Diabet Med 15 (Suppl. 4): S60-S62.
4. The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus:Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. 2000. Diabetes Care Volume 23(suppl 1):S4-S19.
5. Bloomgarden, Z.T. 2000.European Association for the Study of Diabetes Annual Meeting. Diabetes Care Vol 24, No 6. June. 1115-1119.
6. Tuomilehto et al., May 3, 2001. Prevention Of Type 2 Diabetes Mellitus By Changes In Lifestyle Among Subjects With Impaired Glucose Tolerance. Volume 344 Number 18. New England Journal of Medicine.
7. Eriksson KF and F. Lindgarde. 1991. Prevention of type 2 diabetes mellitus by diet and physical exercise:the 6-year Malmo feasibility study. Diabetologia volume 34:891-898.
8. Pan XR et al..1997. Effectsof diet and exercise in preventing NIDDM in people with impaired glucose tolerance: the Da Qing IGT and Diabetes Study. Diabetes Care volume 20:537-544.

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The BC Endocrine Research Foundation Presents a Fall Symposium “What’s New In Midlife Women’s Health”.

• Sunday November 4, 2001 9:30 am Reception, 10:00am Symposium.
• Location: International Ballroom, Delta Pacific Resort and Conference Centre, 10251 St. Edwards Drive, Richmond, BC
• Hosted by Joyce Resin Panel Discussion Questions and Answers
• Presentations :
  • Dr. Diane Finegood — Insulin Resistance and Diabetes Prevention: Research prospects in the new Canadian Institutes of Health Research environment
  • Dr. Jerilynn Prior — What’s New About Perimenopause
  • Andrea Swan — Making Sense of Menopause: What Women Want for Informed Decision Making.

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