Resolving to Quit Smoking?

Three acupuncture sessions for quitting for only $149 (regularly $210).

1. Acupuncture Is Very Effective To Help Stop Smoking.
In a recent study, “Alternative Smoking Cessation Aids: A Meta-analysis of Randomized Controlled Trials,” researchers gathered data from 14 different studies to see which alternative techniques helped patients stop smoking. The acupuncture studies examined 823 different patients. The researchers concluded that both acupuncture and hypnotherapy may help patients quit smoking.
Acupuncture stops jitters, curbs cravings, lessens irritability and restlessness, increases relaxation and helps detoxify the body. It can also restore balance in your constitution and jumpstart the healing process.

2. Acupuncture Can Reduce Cravings, But It Can’t Change Habits.
Physical cravings are only one aspect of cigarette addiction. Many times, the habit of smoking is harder to stop than the physical addiction.
If smoking is part of a daily ritual, not smoking can make your day feel “off.” All of this is normal and challenging. Get rid of the ashtrays, re-arrange your favorite smoking areas to make them smoker unfriendly, get your car detailed and make it smoke free, tell your friends, family and co-workers your quit date. Recruit the smokers closest to you to quit with you.

Use all the support systems you have available. Get help from family and friends. Join a support group. Exercise. Find new smoke-free activities.
Stopping a smoking addiction requires support—physically, emotionally and socially.

3. Supplements Can Help With Cravings.
Smoking, like sugar, raises serotonin levels (one reasons why those who quit smoking gain weight). Serotonin building blocks like 5-HTP help support serotonin levels. We offer pharmaceutical grade 5-HTP sources tailored to your needs.

Avoiding Anemia

Feel tired all the time? You may be anemic!

If you feel tired and weak you may have anemia. When the number of red blood cells or your hemoglobin level is too low, your body can’t get all of the oxygen it needs, this can leave you feeling very tired and may even affect your ability to concentrate. Anemia can also cause shortness of breath, dizziness, headaches, pale skin, or cold hands and feet.

Anemia may be mild and short term but can become serious if left untreated for a long period of time. Anemia is often easily preventable or correctable if it is due to lack of specific nutrients. The most common forms of anemia are blood loss anemia, folic acid deficiency, B12 deficiency and iron deficiency.

Anemia is very common and occurs in all age, racial, and ethnic groups. Both men and women can have anemia although women of childbearing age are at higher risk for anemia due to their menstrual cycles.

In addition to needing iron, folic acid (folate), or vitamin B12 your body also needs small amounts of vitamin C, riboflavin, and copper to make red blood cells. Issues of malabsorption can make it difficult for your body to absorb the nutrients required to making enough red blood cells.

Iron rich foods include beef and other red meats, chicken, turkey, pork, fish, and shellfish, iron-fortified cereals, dark green leafy vegetables, peas; lentils; white, red, and baked beans; soybeans; and chickpeas, prunes, raisins, apricots, prune juice and dried fruit.

Foods rich in folic acid, can be found in citrus fruits and juices, bananas, dark green leafy vegetables, and fortified breads, cereals, and pasta and rice, black-eyed peas and dried beans, beef liver and eggs.

Vitamin B12 is found in clams, liver, beef, fortified breakfast cereals, trout, salmon, tuna, haddock, milk, yogurt, cheese, ham, eggs, and chicken.

Vitamin C helps the body absorb iron. Good sources of vitamin C are vegetables and fruits, especially citrus fruits such as oranges, grapefruits, and tangerines. Fresh and frozen fruits, vegetables, and juices usually have more vitamin C than canned ones. Other fruits rich in vitamin C include kiwi fruit, strawberries, and cantaloupes. Vegetables rich in vitamin C include broccoli, peppers, brussel sprouts, tomatoes, cabbage, potatoes, and leafy green vegetables like turnip greens and spinach.

Riboflavin (Vitamin B2) can be found in fortified cereals and energy bars, spirulina, (dry seaweed), whey, maple syrup, venison, caviar, liver, milk, peas, zucchini, sun dried tomatoes, tempeh (fermented soy), Greek yogurt, bean sprouts, and soymilk.

Copper, a trace mineral, like riboflavin is required for blood formation and, like vitamin C helps the body absorb and use iron. Sources of copper include spirulina, trail mix, quail, tortilla chips, radicchio, soy chips, dried coconut, puffed millet, granola bars, roasted buckwheat, kamut, chestnuts, peanut butter, grape leaves, bacon, salami, paprika, molasses, ground ginger, chili powder, soybean sprouts, medjool dates, and wakame seaweed.

Many people living with anemia may not realize they have it. They might have mild symptoms or none at all. A doctor can determine whether you have anemia by a simple blood test. If you have the symptoms of anemia but are not checked for all these nutrients in your blood testing, you may find you missed the actual cause of your symptoms!

Lack of sleep may cause back pain!

Many adults suffer from lack of sleep and back pain, and University of Haifa researchers who collaborated with colleagues from Tel Aviv Sourasky Medical Center have linked the two ailments for the first time.

“Our findings point to the importance of integrated treatment for the two to prevent back pain and improve the quality of sleep,” the researchers said.

Dr. Ma’ayan Agmon of the university’s nursing department and Dr. Galit Armon of the psychology department, together with Prof. Shlomo Berliner and Prof. Yitzhak Shapira of Sourasky, discovered that lack of sleep actually leads to back pain. Their study looked at 2,131 people with an average age of 46, an average educational level of 15.8 years in school who worked an average of 9.6 hours a day.

The risk of back pain rises significantly among people who suffer from sleep disturbances, they said, adding that they couldn’t be sure how one problem causes the other. We do however know that the neurotransmitters involved in pain are counterbalanced by neurotransmitters involved in sleep.

Among women, the link between sleeplessness and back pain was noted as being even greater.

The authors suggested that one of the reasons lack of sleep and back pain may be connected is due to people with sleep problems describing their lives as being “pressured.” They felt that the chronic lack of rest can lead to muscle tension. It may also be due to malabsorption of B complex vitamins while under stress. B vitamins are essential for the formation of neurotransmitters associated with deep sleep and with correct nerve function (which may impact pain).

“After neutralizing other factors such as socioeconomic levels, lifestyles and more, we reached the conclusion that sleeplessness predicts back pain – but the opposite is not true,” Agmon and Armon said.

A person’s sensitivity to pain rises if that person wakes up too early or spends hours awake instead of sleeping, and often feels pain simultaneously and more powerfully compared to other people.

Schedule an appointment with Dr Crosby at (636)928-5588 to discuss your poor quality sleep and pain issues. Some simple tests and supplements may be all you need to sleep better and feel better!

Inflammation. A Choice?

As you are aware, if you catch a cold your immune system swings into action. Did you know it also becomes involved with a sprained ankle?

Both infection and injury are triggers for inflammation and the familiar heat, pain, redness, and swelling associated with inflammation are also the signs that your immune system is involved!

Inflammation begins when inflammatory hormones in your body activate your white blood cells in order to clean up infected and damaged tissue. These agents are matched by equally powerful, closely related anti-inflammatory compounds, which should be activated once the infection or damaged tissue has been acted on and it is time to begin the healing process.

Acute inflammation is inflammation that comes at the first sign of an injury or infection and leaves the tissue when it is done. This type of response is the sign of a well-balanced immune system. Chronic inflammation however is the same process without the off switch. It literally stays on red alert all the time. Generally, with chronic inflammation, what started as a healthy and normal response, just won’t shut off.

Chronic inflammation has its roots in the digestive system and while there is no definitive test for inflammation we can sometimes identify it by use of tests for C-reactive proteins, fibrinogen, or homocysteine or by testing the erythrocyte sedimentation rate.

Our society is vulnerable to chronic inflammation. Our diet here in the United States of processed food in lieu of unprocessed foods that take a bit more effort to prepare, and our overuse of antibiotics in ourselves and in our meat/dairy are expressed in our rising rates of allergies, obesity, gut health issues, autoimmune diseases, and chronic pain.

The good news is, once we understand what causes inflammation we can start improving our choices and over time minimize our inflammatory response.

The root of chronic inflammation, autoimmune issues and other chronic disease states often start with poor gut health. It is no surprise really that over seventy percent of your body’s immune system resides in your gastrointestinal tract. We were designed this way in order to eliminate viruses and bacteria we might ingest while ensuring the maximum absorption of nutrients. Unfortunately, our current health care model works to mask the symptoms of chronic inflammation, rarely looking at the gut as the true cause behind the symptoms.

Intestinal bloating, frequent bouts of diarrhea or constipation, gas and pain, heartburn and acid reflux are early signs of an unhappy digestive tract and, by default, of an unhappy immune system. Our evolution from the hunter-gatherer diet to the convenience and fast foods of the past century is overwhelming our gut health and ultimately our health and quality of life. Our modern diet offers the wrong essential fatty acids, too much sugar, too many carbohydrates, and extremely high levels of wheat, dairy, and other common allergens.

Foods that cause inflammation

  • Polyunsaturated vegetable oils like safflower, sunflower, corn, peanut and soy are high in omega 6 (inflammatory) fatty acids. These oils contain almost no omega-3s which reduce inflammation.
  • High-carb, low-protein diets. We took proteins and fats out of our diets in the late 1970’s and early 1980’s and have trended for obesity and inflammatory diseases since that time. Low carb diets are generally much healthier.
  • Refined sugar and sugary foods raise insulin levels creating inflammation.
  • Common food allergens will trigger the inflammatory cascade in those sensitive to them. Food sensitivity testing is an easy way to identify what foods to avoid.
  • Foods high in trans fats create LDL’s, or “bad cholesterol”, create inflammation of arteries.

To reduce chronic inflammation you must watch what you consume!
If you are watching your sugar consumption, cooking with the right oils, raising the percentage of fruits/vegetables and unprocessed foods in general while reducing your processed food carbohydrate load, you should see reductions in your inflammatory response over a period of a few weeks. If you have tried this with no appreciable results, you may want to consider that foods you have always eaten (which never seemed to effect you) may now be triggering a low grade allergic response (known as a food sensitivity). Additionally, If you have been on long term antacid use or on many rounds of antibiotics, you may need to consider digestive enzymes or probiotics (supplements containing the “good” bacteria that support healthy digestion) to help your gut health and immune system get back on track so you can naturally lower your inflammation.

But your digestive tract is only the beginning of the story. Let’s take a look at some other causes of chronic inflammation.

Inflammation and menopause
Changing levels of estrogen, progesterone, and testosterone have a role to play in age-related inflammation. We still don’t understand all the connections, but it appears that a decrease in estrogen corresponds with a rise in inflammation. This response is exacerbated by poor Vitamin D levels (Vitamin D is an estrogen regulator.)

Weight gain, around the waist in particular, is another risk of menopause. There is clear evidence that extra fat cells around the trunk raise your risk of inflammation.

If you have ever almost been in a car accident you know the feel of a cold sweat with your heart pounding in your throat. This “fight or flight” response is orchestrated by your nervous system and triggers the release of the stress hormone cortisol from your adrenal glands which are part of your endocrine system.

Cortisol affects both insulin levels and metabolism and It is involved in chronic inflammation. Coping with persistent stress, producing cortisol on a daily basis to deal with the stress, affects your immune system, your adrenals, and your central nervous system. It is important therefore to deal with life stressors as part of dealing with inflammation.

Growing evidence shows that diet and lifestyle can either create a pro-inflammatory environment or an anti-inflammatory one. Here are some everyday steps you can take to cool the heat of inflammation with good nutrition:

    1) Don’t smoke or be around smoke 2) Exercise 3) Identify your physical and emotional stressors and figure out how to improve things to reduce the stress 4) Consume more water 5) Eat a healthy diet including 7 to 9 servings of fruits and vegetables a day

Vegetables such as broccoli, cabbage, Brussels sprouts, kale and cauliflower are high in inflammation minimizing compounds.

Eat fewer foods made with flour and sugar, especially packaged snack foods, as these refined carbohydrates promote inflammation. If you enjoy pasta, eat it in moderation and cook it al dente (firm to the bite).

Favor healthy fats such as extra-virgin olive oil or flax oil.

Include moderate amounts of avocados, nuts and seeds in your meals or snacks.

Avoid heavily processed foods.

Move beyond meat. Fish, with its healthful omega-3 fats, and plant-based proteins like legumes and less-processed forms of soy (tofu, tempeh, edamame, soy milk) can help reduce inflammation.

Spice it up. Spices are more than just flavoring agents — they are also packed with phytochemicals. Ginger and turmeric are particularly noted for their anti-inflammatory properties.

Drink tea, green, oolong and black. They all contain inflammation-fighting phytochemicals although green tea does this best. Herbal teas (unless ginger) don’t have the same benefit

While coffee has inflammation fighting phytochemicals, in excess it can create inflammation.

Eating more calories than your body needs can promote inflammation. If your weight stays fairly steady, you are probably eating the right amount of calories for your level of activity.

Alcohol is inflammatory. If you drink, red wine in moderation is the healthiest option.

To satisfy a sweet tooth, fresh fruit or small amounts of plain dark chocolate are your best bets.

Alcat food sensitivity testing is a great way target specific foods associated with your inflammatory issues. The Yale School of Medicine conducted a study on the Alcat Food Sensitivity Test and found that “identification of activation markers can provide a biological understanding of food sensitivity, and may form the basis for more targeted clinical management.”

Call to set up an appoint to see if Alcat testing is right for you today. (636)928-5588

Weight Loss Relieves Knee Arthritis Pain Symptoms!

Obese patients with knee osteoarthritis (OA) who maintain an initial weight loss report fewer symptoms compared with their baseline level of symptoms, Danish researchers reported in Arthritis Care & Research.

The improvement in symptoms was similar regardless of the weight maintenance program followed; either a dietary intervention, a program of knee exercises, or no formal intervention (controls). The results suggest that weight loss is the key component to knee OA pain relief, according to Henning Bliddal, MD, DMSc, of Copenhagen University Hospital, and colleagues.

The finding, which comes from an assessment of data from CAROT (Cartilage in Obese Knee Osteoarthritis Patients Trial), “confirms the feasibility of long-term weight loss maintenance in sedentary individuals, in this case patients with mobility limitations due to knee OA,” the authors wrote.

The investigators found that those doing exercises for their knee OA with no weight loss did worse than those who lost weight leading them to conclude that diet is mandatory for the weight loss to minimize knee pain from OA.

We can help with weight loss!

Ask our doctors about Ideal Protein or Standard Process as two means of effectively shedding the pounds and the knee pain! (636)28-5588.

Feel tired all the time? You may be anemic even if your doctor has told you otherwise! Your fatigue may not be depression!

If you feel tired and weak most of the time you may have anemia.

Anemia occurs when the number of red blood cells is too low or your hemoglobin level is too low. When this occurs, your body tissues can’t get all of the oxygen they need leaving you feeling very tired and making every activity effortful. Anemia may also affect your ability to concentrate or create a brain fog. It may also cause shortness of breath, dizziness, headaches, pale skin, or cold hands and feet.

Anemia may be mild and short term but can become serious if left untreated for a long period of time. Anemia is often easily preventable or correctable if it is due to lack of specific nutrients. The most common forms of anemia are blood loss anemia, folic acid deficiency, B12 deficiency and iron deficiency anemia.

Anemia is very common and occurs in all age, racial, and ethnic groups. Both men and women can have anemia although women of childbearing age are at higher risk for anemia due to their menstrual cycles.

In addition to needing iron, folic acid (folate), or vitamin B12 your body also needs small amounts of vitamin C, riboflavin, and copper to make red blood cells. Issues of intestinal malabsorption can make it difficult for men, women and even children to absorb these critical nutrients required for making enough red blood cells.

Iron rich foods include beef and other red meats, chicken, turkey, pork, fish, and shellfish, iron-fortified cereals, dark green leafy vegetables, peas; lentils; white, red, and baked beans; soybeans; and chickpeas, prunes, raisins, apricots, prune juice and dried fruit.

Foods rich in folic acid, can be found in citrus fruits and juices, bananas, dark green leafy vegetables, and fortified breads, cereals, and pasta and rice, black-eyed peas and dried beans, beef liver and eggs.

Vitamin B12 is found in clams, liver, beef, fortified breakfast cereals, trout, salmon, tuna, haddock, milk, yogurt, cheese, ham, eggs, and chicken.

Vitamin C helps the body absorb iron. Good sources of vitamin C are vegetables and fruits, especially citrus fruits such as oranges, grapefruits, and tangerines. Fresh and frozen fruits, vegetables, and juices usually have more vitamin C than canned ones.

Other fruits rich in vitamin C include kiwi fruit, strawberries, and cantaloupes.

Vegetables rich in vitamin C include broccoli, peppers, brussel sprouts, tomatoes, cabbage, potatoes, and leafy green vegetables like turnip greens and spinach.

Riboflavin (Vitamin B2) can be found in fortified cereals and energy bars, spirulina, (dry seaweed), whey, maple syrup, venison, caviar, liver, milk, peas, zucchini, sun dried tomatoes, tempeh (fermented soy), Greek yogurt, bean sprouts, and soymilk. Copper, a trace mineral, like riboflavin is required for blood formation and, like vitamin C helps the body absorb and use iron. Sources of copper include spirulina, trail mix, quail, tortilla chips, radicchio, soy chips, dried coconut, puffed millet, granola bars, roasted buckwheat, kamut, chestnuts, peanut butter, grape leaves, bacon, salami, paprika, molasses, ground ginger, chili powder, soybean sprouts, medjool dates, and wakame seaweed.

If your doctor has told you you don’t have anemia but you are experiencing the symptoms of anemia outlined above, there are several questions to be asking your doctor. The first is are your B12/folic acid values in the low normal range? What is your iron level? What is your percent oxygen saturation rate (can your cells actually carry oxygen to tissues).

Researchers agree that there is a considerable population who experience all the symptoms of anemia when in the low normal range with their B12/folic acid. If iron isn’t checked, your B12/folic acid may look normal but you may have iron deficiency anemia. Beyond this, there are other concerns that should be raised. Are your copper levels adequate? Most doctors do not check for copper levels or vitamin C levels.

Finally, your fatigue may not be anemia or depression. It may be a subclinical thyroid issue. With breads now being manufactured with bromine and people migrating to sea salt and kosher salt, iodine deficiency is silently impacting energy without necessarily impacting T3 or T4 numbers adequately enough to be detected with standard thyroid testing.

Many people living with fatigue do not realize they have anemia. They certainly never imaging they might be iodine deficient. All of these simple blood tests are generally covered by insurance and, are verily easily treated once identified as abnormal. If you have symptoms of anemia but are not checked for all these conditions in your blood testing, you may have actually missed the cause of your symptoms!

Acupuncture for Infertility

When used in conjunction with Western fertility treatments, acupuncture increases conception rates by 26%. A recent study from Tel Aviv University reports, ““When combining IUI with TCM treatments, 65.5 percent of the test group were able to conceive, compared with 39.4 percent of the control group, who received no herbal or acupuncture therapy.” For the 4.5 million couples experiencing infertility each year, acupuncture may be just what the doctor ordered.

Acupuncture can increase fertility by reducing stress, increasing blood flow to the reproductive organs and balancing the endocrine system, according to several studies and medical research. “The goal of an infertility treatment from a Chinese Medicine perspective is not just to get pregnant, but to stay pregnant and to have a healthy baby,” says Deb Davies, LAc, a Pacific College alumnus who practices at Herbin Acupuncture and Wellness in San Diego. Among many other benefits, acupuncture can provide better blood flow to the ovaries and uterus, creating a stronger chance for an egg to be nourished and carried to term.

Acupuncture consists of the gentle insertion and stimulation of thin, disposable sterile needles at strategic points near the surface of the body. Over 2,000 acupuncture points on the human body connect with 14 major pathways, called meridians. Chinese medicine practitioners believe that these meridians conduct qi , or energy, between the surface of the body and internal organs. It is qi that regulates spiritual, emotional, mental and physical balance. When the flow of qi is disrupted through poor health habits or other circumstances, pain and/or disease can result. Acupuncture helps to keep the normal flow of this energy unblocked, thereby increasing a couple’s chances of conceiving.

Acupuncture infertility treatment can improve almost every cause of this obstacle. While 40 percent of infertility is caused by problems in the female, another 40 percent is caused by problems in the male, such as low sperm count or motility. The cause of female infertility stems from problems such as anovulation and endometriosis. The remaining 20 percent is caused by unknown factors.

One of the ways acupuncture infertility treatment increases fertility is by reducing stress, which is often a key factor in the fertility of both men and women. When people are under stress, the hormone cortizol is released in the brain. This alters the brain’s neurochemical balance, thus changing hormone levels and disrupting the pituitary balance that is key to the reproductive cycle. “Chinese medicine can help support a woman through this important time in her life—whether that is emotionally or physically, acupuncture can help with much more than just conception. It can help with morning sicknesss, nausea, aches and pains (low back pain, for example), anxiety preparation for birth, and insomnia, among many others,” explains Davies.

Because of the delicate balance between the hypothalamus, pituitary, and reproductive glands, stress is capable of preventing a woman from ovulating entirely. This can contribute to the cause of female infertility. Stress can also create spasms in both the fallopian tubes and the uterus, which can interfere with movement and implantation of a fertilized egg. In men, stress can alter sperm counts, motility, and cause impotence. Acupuncture infertility treatment counters the effects of stress and cortizol by releasing endorphins in the brain. An herbal impotence cure is also an option for men and can reduce stress.

Hormonal balance does not have to be disrupted by cortizol to cause infertility. The most common cause of female infertility is an ovulation disorder, in which the release of a mature egg from the ovary is prevented, usually because of a hormonal imbalance. Without enough progesterone, for example, the fetus is unable to attach to the uterus. High levels of prolactin, the hormone that stimulates the production of breast milk, can also prevent ovulation.

An imbalance in reproductive hormones can also negatively affect male reproductive function, such as sperm motility and production. However, the fertility drugs that stimulate ovulation in women by regulating the hypothalamus and pituitary, the glands that control reproductive hormones, don’t perform nearly as well for men (success rates are about a third of those for women), nor have they been approved for men by the FDA. Male infertility treatment must take another track. An herbal impotence cure — if impotence is a factor in a couple’s infertility — causes no side effects and has a reported success rate when taken in conjunction with male infertility treatment.

While the fertility drugs commonly prescribed for women can produce a 20 to 60 percent pregnancy rate, they also commonly include such side effects as abdominal tenderness, bloating, fluid retention, weight gain, and nausea. Some studies show that they may also cause breast cancer. Acupuncture infertility treatment, by contrast, produces few or no side effects while performing the same function as the drugs do: stimulating the hypothalamus to effectively balance the endocrine system and its hormones and to get to the root cause of female infertility as well as male infertility.

SOURCES Tel Aviv University study;id=15808 – See more at:

Taking NSAIDs during pregnancy Is it safe?

Karen Jackson-Northey Michael F. Evans, MD, CCFP

Nielsen GL, Sorensen HT, Larsen H, Pedersen L. Risk of adverse birth outcome and miscarriage in pregnant users of non-steroidal anti-inflammatory drugs: population based observation study and case-control study. BMJ 2001;322(7281):266-70.
Research question

Are nonsteroidal anti-inflammatory drugs (NSAIDs) associated with adverse fetal outcomes when taken during pregnancy? Specifically, is there risk of miscarriage, congenital abnormalities, low birth weight, or prematurity?

Type of article and design
Population-based primary research article using both cohort and case-control designs.

Relevance to family physicians
Anti-inflammatories are thought to be one of the most commonly prescribed drugs during pregnancy.1 A recent study of 101 newborns in Michigan showed that 49.5% had NSAIDS detected in their meconium.2 Given the high use of both prescription and over-the-counter NSAIDs, knowledge of any adverse effects of taking them during pregnancy is important for family doctors.

To date, acetylsalicylic acid (ASA) has been the most thoroughly studied NSAID. The general (but not unanimous) consensus is that low-dose (<3 g/d) ASA is not associated with increased risk of congenital anomalies, prematurity, low birth weight, or miscarriages.3 Research on other NSAIDs, however, particularly the newer cyclooxygenase-2 inhibitors, is scant, with very few population-based studies.
Some current articles in the literature recommend stopping NSAIDS 6 to 8 weeks before delivery.4,5 This reduces the possible risk of early closure or constriction of the ductus arteriosus, persistent fetal pulmonary hypertension, intracranial hemorrhages, andrenal toxicity in fetuses.2,4 This study did not address these end points.

Overview of study and outcomes
The study was based in a Danish community, where a central pharmacy database kept records of all reimbursed prescription drugs (including NSAIDs equivalent to >400 to 600 mg of indomethacin). The local birth registry and hospital discharge summaries were the sources of the rest of the raw data.

The cohort study compared pregnancies where mothers had used NSAIDs (n = 1462) with pregnancies where they had not (n = 17 259) and looked at the incidence of birth defects, prematurity, and low birth weight. Pregnancies where mothers had used NSAIDs early (30 days before conception until end of first trimester) were analyzed for risk of congenital anomalies; pregnancies where mothers had used NSAIDs late (ie, during second or third trimester) were analyzed for low birth weight (<2500 g) or prematurity (birth at <37 weeks). Logistic analysis was used to calculate odds ratios (OR), and adjustments were made for mothers’ age, smoking status, and birth order.

In the case-control study, miscarriages in pregnancies with or without NSAID use in the first trimester (63/4268) were compared with live births with or without NSAID use in the third trimester (318/29 750). Data were grouped according to time between NSAID purchase and discharge from hospital (1, 2 to 3, 4 to 6, 7 to 9, and 10 to 12 weeks). Again, logistic analysis was used to calculate ORs, and adjustments were made for mothers’ age.

In the cohort study, there was no statistical association between filling NSAID prescriptions and risk of congenital abnormalities, low birth weight, or preterm birth. In fact, no specific trend in anomalies was noted. The case-control study, however, showed significant risk of miscarriage. A general trendindicated higher risk associated with filling prescriptions closer to time of miscarriage. The OR for 1 week between NSAID purchase and discharge after miscarriage was 6.99 (95% confidence interval [CI] 2.75 to 17.54); the OR for 10 to 12 weeks between purchase and discharge was 1.26 (95% CI 0.85 to 1.87).

Analysis of methodology
This type of trial is lower in the hierarchy of scientific investigation, but the only method available in this case. It would be impossible ethically to investigate adverse fetal effects using a randomized controlled trial. The strengths of this study included a large population sample with no selection bias and pharmacy and discharge summary databases validated through other studies.

Because the study was done retrospectively, the authors were confined to hard end points and database constraints. This meant that over-the-counter purchases of NSAIDs were not accounted for; the various types of NSAIDs were not differentiated; and prescription filling, rather than actual consumption of drugs,was the independent variable. Researchers assumed that, once a prescription was filled, the drug was taken.

Regarding the observation of a higher incidence of miscarriages with NSAID use closer to time of miscarriage, it is unclear whether the pain of miscarriage increased use of NSAIDs or whether the drug itself caused the event. It is possible that women with disease requiring NSAIDs during pregnancy have a higher incidence of miscarriages regardless of drug use. Last, the database in this study did not include mothers’ smoking status, which could confound results.

Application to clinical practice
While this study showed an association between miscarriage and NSAID use, there are several alternative explanations of the observed correlation and several possible confounding factors. As the authors conclude, the result is a new observation and needs further research to investigate a possible causative link. It is worth our noting NSAID use by patientswho have miscarriages and informing them of this recently published observation.
The cohort study lends additional support to the safety of NSAIDS regarding teratogenicity and risk of prematurity or low birth weight. Patients can be reassured on this issue.
The study did not investigate incidence of persistent pulmonary hypertension of newborns, ductus arteriosus constriction, renal dysfunction or toxicity, or bleeding, all of which have been linked with NSAID use during pregnancy.

Bottom line
• Using NSAIDs during early or late stages of pregnancy is not associated with congenital anomalies, prematurity, or low birth weight.
• There is a significant link between NSAID use and miscarriage in the first trimester. This association could be secondary to underlying disease caused by NSAID use or caused by the pain of miscarriage.
• Further research is needed.


1. Bonati M, Bortolus R, Marchetti F, Romero M, Tognoni G. Drug use in pregnancy: an overview of epidemiological (drug utilization) studies. Eur J Clin Parmacol 1990;38(4):325-8.
2. Alano MA, Ngougmna E, Ostrea EM Jr, Konduri GG. Analysis of nonsteroidal antiinflamatory drugs in meconium and its relation to persistent pulmonary hypertension of the newborn. Pediatrics 2001;107(3):519-23.
3. CLASP: a randomised trial of low-dose aspirin for the prevention and treatment of pre-eclampsia among 9364 pregnant women. CLASP (Collaborative Low-dose Aspirin Study in Pregnancy) Collaborative Group. Lancet 1994;343(8898):619-29.
4. Janssen NM, Genta MS. The effects of immunosuppressive and anti-inflammatory medications on fertility, pregnancy and lactation. Arch Intern Med 2000;160(5):610-9.
5. Ostensen M, Ramsey-Goldman R. Treatment of inflammatory rheumatic disorders in pregnancy: what are the safest treatment options? Drug Saf 1998;19(5):389-410.

Nutrition and Fertility

Eur J Endocrinol. 2012 May;166(5):765-78. doi: 10.1530/EJE-11-0984. Epub 2012 Jan 24.

Vitamin D and fertility: a systematic review.

Lerchbaum E1, Obermayer-Pietsch B.
Author information

Vitamin D has been well-known for its function in maintaining calcium and phosphorus homeostasis and promoting bone mineralization. There is some evidence that in addition to sex steroid hormones, the classic regulators of human reproduction, vitamin D also modulates reproductive processes in women and men.

The aim of this review was to assess the studies that evaluated the relationship between vitamin D and fertility in women and men as well as in animals.

We performed a systematic literature search in Pubmed for relevant English language publications published until October 2011.


The vitamin D receptor (VDR) and vitamin D metabolizing enzymes are found in reproductive tissues of women and men. Vdr knockout mice have significant gonadal insufficiency, decreased sperm count and motility, and histological abnormalities of testis, ovary and uterus. Moreover, we present evidence that vitamin D is involved in female reproduction including IVF outcome (clinical pregnancy rates) and polycystic ovary syndrome (PCOS). In PCOS women, low 25-hydroxyvitamin D (25(OH)D) levels are associated with obesity, metabolic, and endocrine disturbances and vitamin D supplementation might improve menstrual frequency and metabolic disturbances in those women. Moreover, vitamin D might influence steroidogenesis of sex hormones (estradiol and progesterone) in healthy women and high 25(OH)D levels might be associated with endometriosis. In men, vitamin D is positively associated with semen quality and androgen status. Moreover, vitamin D treatment might increase testosterone levels. Testiculopathic men show low CYP21R expression, low 25(OH)D levels, and osteoporosis despite normal testosterone levels.

Int J Fertil. 1991 Jan-Feb;36(1):36-8.

Vitamin B12 deficiency and infertility: report of a case.

Sanfilippo JS1, Liu YK.
Author information

An oligomenorrheic infertile patient with evidence of vitamin B12 (cobalamin) deficiency is described. Treatment consisted of clomiphene citrate, human chorionic gonadotropin (hCG), conjugated estrogens, dexamethasone, and ferrous sulfate. Pregnancy occurred after 1,000 micrograms of vitamin B12 was added to the treatment regimen. We believe the patient’s infertility was in part related to the megaloblastic anemia. A possible correlation between vitamin B12 deficiency and failure to ovulate is presented.

Andrologia. 2009 Feb;41(1):46-50. doi: 10.1111/j.1439-0272.2008.00895.x.

Prevalence of low serum cobalamin in infertile couples.

Pront R1, Margalioth EJ, Green R, Eldar-Geva T, Maimoni Z, Zimran A, Elstein D.

A high prevalence of low levels of cobalamin (B12) had been found in a survey of multi-ethnic normal individuals in Israel. The purpose of this study was to investigate the incidence of cobalamin deficiency among Israeli couples suffering from infertility. All couples seen at the in vitro fertilization clinic at an urban hospital (Shaare Zedek Medical Center) in Jerusalem for a 6-month period were invited. Mean cobalamin levels were 259.2 pg ml(-1) in males and 275.1 pg ml(-1) in females (normal >200 pg ml(-1)), 35.5% of 172 men and 23.3% of 223 females had cobalamin deficiency (P = 0.01). There were 171 couples with complete demographic questionnaires and cobalamin values for each partner. In 74 couples (43.3%), one partner was cobalamin deficient, with no significant difference between those with unexplained infertility versus those with explained infertility; and in 13 couples, both partners were cobalamin deficient. Thirty-nine per cent of all men with an abnormal semen analysis had cobalamin deficiency, a finding that requires further investigation. This study questions whether higher rates of male infertility in Israel are partially ascribable to cobalamin deficiency. Recommendation for supplementation in both males and females to achieve high-normal levels of cobalamin would be prudent.
Int J Gen Med. 2011; 4: 99–104.
Published online 2011 Jan 23. doi:  10.2147/IJGM.S16275
PMCID: PMC3048346

Selenium–vitamin E supplementation in infertile men: effects on semen parameters and pregnancy rate

Mohammad K Moslemi1,2 and Samaneh Tavanbakhsh3
This article has been cited by other articles in PMC.




Infertility is an important medical and social problem that has an impact on well-being. A significant development in the last 10 years in the study of human infertility has been the discovery that oxidative sperm DNA damage has a critical role in the etiology of poor semen quality and male infertility. Selenium (Se) is an essential element for normal testicular development, spermatogenesis, and spermatozoa motility and function. The predominant biochemical action of Se in both humans and animals is to serve as an antioxidant via the Se-dependent enzyme glutathione peroxidase and thus protect cellular membranes and organelles from peroxidative damage. We explored the efficacy of Se in combination with vitamin E for improving semen parameters and pregnancy rates in infertile men.

Clin Endocrinol (Oxf). 2012 Sep;77(3):343-50. doi: 10.1111/j.1365-2265.2012.04434.x.

Vitamin D in the aetiology and management of polycystic ovary syndrome.

Thomson RL1, Spedding S, Buckley JD.

Vitamin D deficiency is common in women with polycystic ovary syndrome (PCOS), with the 67-85% of women with PCOS having serum concentrations of 25-hydroxy vitamin D (25OHD) <20 ng/ml. Vitamin D deficiency may exacerbate symptoms of PCOS, with observational studies showing lower 25OHD levels were associated with insulin resistance, ovulatory and menstrual irregularities, lower pregnancy success, hirsutism, hyperandrogenism, obesity and elevated cardiovascular disease risk factors. There is some, but limited, evidence for beneficial effects of vitamin D supplementation on menstrual dysfunction and insulin resistance in women with PCOS. Vitamin D deficiency may play a role in exacerbating PCOS, and there may be a place for vitamin D supplementation in the management of this syndrome, but current evidence is limited and additional randomized controlled trials are required to confirm the potential benefits of vitamin D supplementation in this population.

© 2012 Blackwell Publishing Ltd.


Reprod Biomed Online. 2014 Jun;28(6):743-7. doi: 10.1016/j.rbmo.2014.01.019. Epub 2014 Feb 25.

Role of dehydroepiandrosterone in improving oocyte and embryo quality in IVF cycles.

Zangmo R1, Singh N2, Kumar S1, Vanamail P1, Tiwari A1.

The purpose of this study was to evaluate the role of dehydroepiandrosterone (DHEA) on the number and quality of oocytes and embryos in poor responders undergoing IVF cycles. A total of 50 patients with a history of poor ovarian response in the previous cycle(s) were enrolled in a prospective cohort study. They were treated with oral micronized DHEA 25mg three times a day for 4 months. Oocyte and embryo number and quality were recorded before and after treatment. The results were analysed using Student’s paired t-test. After treatment with DHEA, a significant increase in number of mature follicles was seen in the post treatment period (⩽ 35 years P<0.001; ⩾ 36 years P = 0.002). There were significant increases in numbers of oocytes retrieved, fertilization rates and, consequently, the total number of embryos available. More embryos were vitrified among patients ⩽ 35 years (P<0.001) post treatment, and clinical pregnancy rate in this group was 26.7%. DHEA treatment resulted in a higher number of oocytes retrieved, oocytes fertilized, embryos overall and of grade-I embryos. It can help in increasing pregnancy rate in poor responders. This study was performed to evaluate the role of dehydroepiandrosterone (DHEA) treatment on the number and quality of oocytes and embryos in poor responders undergoing IVF cycles. Fifty patients with a history of poor ovarian response in the previous cycle(s) were enrolled in the study and a prospective cohort study was performed. Patients were prescribed oral micronized DHEA 25mg three times a day for 4 months. Oocytes and embryos in terms of both number and quality were measured before and after treatment. A significant increase in mean number of mature follicles was seen in the post-treatment group. There was a significant increase in the number of oocytes retrieved, fertilization rates and, consequently, in the total number of embryos available after treatment with DHEA. More embryos were vitrified post treatment and the overall pregnancy rate was 20%. DHEA resulted in a significant improvement in the numbers of oocytes retrieved, oocytes fertilized, embryos and grade-I embryos. DHEA can help improve pregnancy rate in poor responders with history of previous failed IVF cycles.

J Assist Reprod Genet. 2007 Dec; 24(12): 629–634.
Published online 2007 Dec 11. doi:  10.1007/s10815-007-9178-x
PMCID: PMC3454995

Update on the use of dehydroepiandrosterone supplementation among women with diminished ovarian function

David Barad,corresponding author1,2,5,6 Hyama Brill,3,5,6 and Norbert Gleicher4,5,6

This article has been cited by other articles in PMC.

We assessed the role of DHEA supplementation on pregnancy rates in women with diminished ovarian function.

This is a case control study of 190 women with diminished ovarian function. The study group includes 89 patients who used supplementation with 75 mg daily of oral, micronized DHEA for up to 4 months prior to entry into in vitro fertilization (IVF). The control group is composed of 101 couples who received infertility treatment, but did not use DHEA. The primary outcome was clinical pregnancy after the patient’s initial visit. We developed a Cox proportional hazards model to compare the proportional hazards of pregnancy among women using DHEA with the controls group.

Cumulative clinical pregnancy rates were significantly higher in the study group (25 pregnancies; 28.4% vs. 11 pregnancies; 11.9%; relative hazard of pregnancy in study group (HR 3.8; 95% CI 1.2–11.8; p < 0.05).


DHEA treatment resulted in significantly higher cumulative pregnancy rates. These data support a beneficial effect of DHEA supplementation among women with diminished ovarian function.

Keywords: Dehydroepiandrosterone, Diminished ovarian reserve, Infertility, In vitro fertilization, Pregnancy rates, Age, Life table analysis


Med J Armed Forces India. 2015 Jul;71(3):274-7. doi: 10.1016/j.mjafi.2014.12.022. Epub 2015 Feb 25.

Dehydroepiandrosterone: A panacea for the ageing ovary?

Naredi N1, Sandeep K2, Jamwal VD3, Nagraj N4, Rai S4.


Considerable improvements and advancements have been made in the treatment of infertility but poor ovarian reserve whether due to prematurely or a physiologically ageing ovary, continues to be one of the few unresolved problems of modern infertility care. Fertility researchers had been active for quite some time to find a way to help reverse the effects of ageing on the ovaries but none made an impact till the introduction of Dehydroepiandrosterone [DHEA]. DHEA a mild, and therapeutically well tolerated, male hormone has emerged as a real potential candidate to reverse the effects of ageing on ovaries. Apart from this, DHEA has also been postulated to improve egg and embryo quality, pregnancy rates and time to conception and reduces miscarriage rates. This review attempts to highlight the mechanism of action of this drug, its indications and its current status for treating women with decreased ovarian reserve.


DHEA; Dehydroepiandrosterone; Premature ovarian ageing

PMID: 26288496 [PubMed] PMCID: PMC4534532 [Available on 2016-07-01]

J Steroid Biochem Mol Biol. 2015 Jan;145:213-25. doi: 10.1016/j.jsbmb.2014.06.003. Epub 2014 Jul 5.


Goodarzi MO1, Carmina E2, Azziz R3.


Approximately 20-30% of PCOS women demonstrate excess adrenal precursor androgen (APA) production, primarily using DHEAS as a marker of APA in general and more specifically DHEA, synthesis. The role of APA excess in determining or causing PCOS is unclear, although observations in patients with inherited APA excess (e.g., patients with 21-hydroxylase deficient congenital classic or non-classic adrenal hyperplasia) demonstrate that APA excess can result in a PCOS-like phenotype. Inherited defects of the enzymes responsible for steroid biosynthesis, or defects in cortisol metabolism, account for only a very small fraction of women suffering from hyperandrogenism or APA excess. Rather, women with PCOS and APA excess appear to have a generalized exaggeration in adrenal steroidogenesis in response to ACTH stimulation, although they do not have an overt hypothalamic-pituitary-adrenal axis dysfunction. In general, extra-adrenal factors, including obesity, insulin and glucose levels, and ovarian secretions, play a limited role in the increased APA production observed in PCOS. Substantial heritabilities of APAs, particularly DHEAS, have been found in the general population and in women with PCOS; however, the handful of SNPs discovered to date account only for a small portion of the inheritance of these traits. Paradoxically, and as in men, elevated levels of DHEAS appear to be protective against cardiovascular risk in women, although the role of DHEAS in modulating this risk in women with PCOS remains unknown. In summary, the exact cause of APA excess in PCOS remains unclear, although it may reflect a generalized and inherited exaggeration in androgen biosynthesis of an inherited nature.

Copyright © 2014 Elsevier Ltd. All rights reserved.

AbstractSend to:

Trends Endocrinol Metab. 2011 Mar;22(3):103-9. doi: 10.1016/j.tem.2010.12.002. Epub 2011 Feb 1.

Metabolic syndrome and oocyte quality.

Cardozo E1, Pavone ME, Hirshfeld-Cytron JE.

Metabolic syndrome affects one in four women in the USA, and the incidence is rising every year. Metabolic syndrome is strongly associated with development of coronary artery disease and diabetes. Women of reproductive age are not spared from the complications of metabolic syndrome, which overlaps with obesity and polycystic ovary syndrome (PCOS), both of which are linked to infertility and poor reproductive outcome. Therefore, the relationship between the metabolic syndrome and reproductive dysfunction is an active area of study. In this review, we discuss the animal and human data available to determine if the abnormality is at the level of the ovary and/or endometrium, and discuss the underlying mechanisms causing the associated poor reproductive outcomes.

Copyright © 2010 Elsevier Ltd. All rights reserved.


PMID: 21277789 [PubMed – indexed for MEDLINE]


BMJ. 1998 Aug 1; 317(7154): 329–332.

PMCID: PMC1113632

Fortnightly Review

Polycystic ovarian syndrome: the metabolic syndrome comes to gynaecology

Zoe E C Hopkinson, clinical research fellow,a Naveed Sattar, specialist registrar in clinical biochemistry,b Richard Fleming, consultant grade biochemist,a and Ian A Greer, Muirhead professor of obstetrics and gynaecologya

This article has been cited by other articles in PMC.

Polycystic ovarian syndrome is the most common form of anovulatory infertility.1 Its association with menstrual disturbance and altered hormonal parameters leads many affected women of reproductive age to attend a gynaecology or infertility clinic. The aetiology of the condition is unknown, but recent evidence suggests that the principal underlying disorder is one of insulin resistance, with the resultant hyperinsulinaemia stimulating excess ovarian androgen production. Associated with the prevalent insulin resistance, these women exhibit a characteristic dyslipidaemia and a predisposition to non-insulin dependent diabetes and cardiovascular disease in later life. Thus, polycystic ovarian syndrome seems to have many of the hallmarks of the metabolic syndrome.2–4 This article focuses on the recent change in attitudes to polycystic ovarian syndrome arising from the link with insulin resistance—a concept that not only has major implications for the health of affected women but also offers a potential for new treatments.


Summary points
It is evident that polycystic ovarian syndrome should no longer be considered a purely gynaecological disorder

Affected women seem to have subclinical insulin resistance and a form of the metabolic syndrome that manifests itself in early adult life with gynaecological symptoms

They may therefore gain particular benefit from early screening for cardiovascular risk factors, particularly glucose intolerance

Intervention with insulin sensitising agents, such as metformin, may play a major role in the future treatment of this condition, with the potential capacity to improve both endocrine and metabolic disturbances and reduce the risk of vascular disease

This approach may replace therapies used to treat individual components of polycystic ovarian syndrome such as hirsutism which may reflect a “downstream” feature of this complex metabolic syndrome


Diabetologia. Author manuscript; available in PMC 2015 Jun 1.
Published in final edited form as:
Diabetologia. 2015 Apr; 58(4): 707–715.

Published online 2015 Jan 18. doi:  10.1007/s00125-015-3493-z

PMCID: PMC4416980


History of infertility and risk of type 2 diabetes mellitus: a prospective cohort study

Deirdre K. Tobias,1,2 Audrey J. Gaskins,2,3 Stacey A. Missmer,3,4,5 Frank B. Hu,2,3,4 JoAnn E. Manson,1,3 Germaine M. Buck Louis,6 Cuilin Zhang,6 and Jorge E. Chavarro2,3,4



We sought to evaluate the relationship between delayed conception and type 2 diabetes risk, given that there are plausible underlying mechanisms linking the two, including inflammation and insulin resistance.

Participants of the Nurses’ Health Study II prospective cohort were included if they were free of chronic disease (cardiovascular disease, type 2 diabetes, cancer) at baseline. Biennial questionnaires updated information on infertility status (>12 months attempted pregnancy), lifestyle characteristics and several health-related outcomes. Self-reported cases of diabetes were confirmed using a follow-up questionnaire. Multivariable Cox proportional hazards models were used to compute the HRs and 95% CIs).

Incident type 2 diabetes occurred in 5,993 of the 112,106 participants over 24 years of follow-up (1989–2013). A history of infertility was reported in 27,774 (24.8%) women and was associated with a 20% greater risk of developing diabetes, compared with those never reporting infertility (HR 1.20 [95% CI 1.14, 1.28]), after adjusting for age, lifestyle factors, marital status, oral contraceptive use, family history of diabetes and BMI. Compared with women without a history of infertility, the causes of infertility associated with a higher diabetes risk were ovulation disorders (HR 1.43 [95% CI 1.29, 1.58]) and tubal factor (HR 1.34 [95% CI 1.13, 1.58]). Cervical factor (HR 1.06 [95% CI 0.81, 1.40]) and endometriosis (HR 1.06 [95% CI 0.89, 1.27]) were not associated, while male factor infertility was associated with a modestly higher diabetes risk (HR 1.15 [95% CI 1.00, 1.33]).


These novel findings suggest a history of infertility, particularly that related to ovulation disorders and tubal blockage, is significantly associated with a higher risk of type 2 diabetes.

Keywords: Epidemiology, Fertility, Gestational diabetes, Infertility, Life course epidemiology, Ovulatory disorders, Prospective cohort, Reproductive health, Type 2 diabetes

BMJ. 2006 Feb 25; 332(7539): 434–435.

doi:  10.1136/bmj.332.7539.434

PMCID: PMC1382524

Should obese women with polycystic ovary syndrome receive treatment for infertility? Given the risks such women will face in pregnancy, they should lose weight first?

Adam H Balen, professor of reproductive medicine and surgery

General Infirmary, Leeds LS2 9NS

(Email: ku.shn.htsdeel@nelab.mada)

Martin Dresner, consultant anaesthetist, Eleanor M Scott, senior lecturer in diabetes and endocrinology, and James O Drife, professor of obstetrics and gynaecology

General Infirmary, Leeds LS2 9NS

This article has been cited by other articles in PMC.

Polycystic ovaries are seen at ultrasound in 20-25% of women, and the prevalence of polycystic ovary syndrome (PCOS) seems to be rising because of the current epidemic of obesity.1 The syndrome accounts for 90-95% of women who attend infertility clinics with anovulation. The considerable risks in pregnancy associated with obesity are not usually appreciated when patients with PCOS attend clinics and request fertility treatment. Is it appropriate to offer treatment or to insist on weight loss? Or does any overweight woman have the right to receive treatment, irrespective of the possible outcome?

The syndrome is defined by any two out of the following criteria: infrequent or absent menstruation, indicating anovulation; hyperandrogenism; and polycystic ovaries diagnosed by ultrasound after the exclusion of other aetiologies of menstrual disturbance and hyperandrogenism.2 At least 40% of women with PCOS are obese,1 and they are more insulin resistant than weight matched women with normal ovaries. Increasing abdominal obesity is correlated with reduced menstrual frequency and fertility, together with greater insulin resistance.1,3

Pregnancy carries considerable risks for women who are obese; these include increased rates of congenital anomalies (neural tube and cardiac defects), miscarriage, gestational diabetes, hypertension, and problems during delivery.4,5 Pregnancy exacerbates any underlying insulin resistance, and as a result women with PCOS and obesity have an increased risk of gestational diabetes.6

Increasingly many of these young women also have type 2 diabetes. If the diabetes is diagnosed before conception, patients are often treated for the coexistent features of the metabolic syndrome with statins, angiotensin converting enzyme (ACE) inhibitors, metformin, and thiazolidinediones, all of which are contraindicated in pregnancy. Because these women have irregular menstruation it is not uncommon, if they do conceive, for them not to realise until after organogenesis has occurred. Unfortunately type 2 diabetes is still commonly regarded as being “mild diabetes” but the outcomes of pregnancy in women with type 2 diabetes are much worse than in the general population and are at least equivalent to, if not slightly worse than, in women with type 1 diabetes.7

Overweight mothers are more likely than others to have hypertension and thromboembolism, leading to a higher risk of maternal mortality. In 2000-2, of the 261 deaths reported to the UK Confidential Enquiry into Maternal Health,8 78 women (35%) were obese, compared with 23% of women in the general population, and of these more than a quarter had a body mass index greater than 35. Some of the women who died were so obese that they required special equipment for delivery or special arrangements for caesarean section because their weight exceeded the maximum for the operating table.8

Several studies have shown that weight loss in women with PCOS improves the endocrine profile, the menstrual cycle, the rate of ovulation, and the likelihood of a healthy pregnancy.9 Even a modest loss of 5% of total body weight can achieve a reduction of central fat, an improvement in insulin sensitivity, and restoration of ovulation. Lifestyle modification is clearly a key component for the improvement of reproductive function in overweight women with anovulation and PCOS.10

Such women should be encouraged to lose weight before having treatments to induce ovulation (such as clomifene citrate or gonadotrophins), both to improve the likelihood of ovulation and to enhance ovarian response. Monitoring treatment is also harder in obese women because their ovaries are more difficult to see on ultrasound scans, thus raising the risk of missing multiple ovulation and multiple pregnancy. National guidelines in the United Kingdom for managing overweight women with PCOS advise weight loss, preferably to a body mass index of less than 30, before starting drugs for ovarian stimulation.10

The use of insulin lowering or sensitising agents has excited much interest in the management of PCOS. Metformin inhibits hepatic production of glucose, thereby decreasing insulin secretion, and enhances insulin sensitivity in cells. A systematic review concluded that metformin benefits women with PCOS by reducing serum insulin concentrations and thereby lowering androgen levels, facilitating ovulation, and improving reproductive outcomes.11 Metformin seems to be less effective for women with anovulation and extreme obesity, although perhaps a higher dose is required than currently prescribed.12

Many obese women who wish to conceive are now prescribed metformin, often at body weights greater than would be permissible for treatment to induce ovulation. Those who ovulate and conceive while remaining obese will have to face considerable additional risks during pregnancy. Is it ethical to treat these women with metformin unless they have already lost weight? At the very least the risks of the pregnancy to mother and child should be explained, understood, and actively managed before embarking on treatment. The importance of encouraging and achieving weight loss as first line treatment cannot be overestimated. We suggest that women with obesity and PCOS should defer even treatment with metformin until they reach a target body mass index of 35 or less.