Weight Gain in PeriMenopause & PostMenopause

Good post on how estrogens, when they are reduced by perimenopause and menopause, lower your metabolic rate. Unfortunately, this can start at early as age 35-40. Welcome to Perimenopause, My Friends! But there are things we can do about it. Read on....

Question: Does exercise attenuate or prevent the weight gain that occurs during peri- and post-menopause?

Commentary from:
Wendy M. Kohrt, PhD
Professor of Medicine
University of Colorado, Denver
in Menopause E-consult by the North American Menopause Society

The short answer is, yes, exercise can attenuate
or prevent weight gain during peri- and
postmenopause. The prevention of weight gain
at any age requires only that energy intake not
exceed energy expenditure. Thus, it is possible
to maintain body weight by modifying exercise
and/or eating habits. However, although simple
in theory, there are physiologic changes that
make it particularly challenging for middle-aged
women to maintain energy balance (ie, intake =
expenditure). Because the menopause transition
occurs over a number of years, it is difficult to
determine whether the increased propensity for
weight gain at midlife is primarily a
consequence of the menopause transition or of
advancing age. Both involve factors that make
weight maintenance a challenge.

Menopause-related factors that promote weight
gain. Studies of laboratory animals provide
compelling evidence that estrogen plays an
important role in the regulation of body weight.
Oophorectomy has consistently been found to
cause excess weight gain, and this is prevented
by estrogen replacement.1 There appear to be
multiple mechanisms by which estrogen
deficiency leads to weight gain in animals,
including increased food intake, decreased
spontaneous physical activity, and a suppression
of metabolic rate. If such effects of estrogen
deficiency also occur in humans, this would
suggest that there is a “biological drive” around
the time of menopause toward weight gain.

In fact, there is evidence that estrogen regulates
body weight in women. A number of large,
randomized, placebo-controlled, and open-label
trials of estrogen-based hormone therapy (HT)
have provided strong evidence that weight gain
and, more specifically, fat gain, is attenuated in
women on HT when compared to women on
placebo or no HT.2 Suppressing sex hormone
levels in premenopausal women with
gonadotropin-releasing hormone (GnRH)
agonist therapy also causes fat gain. For
example, women treated for 16 weeks with a
GnRH agonist gained 1.0 kg of fat, which
equates to an energy excess of about 80 kcal per
day.3 Because it is difficult to accurately
measure changes in energy intake and
expenditure of this magnitude in humans, it is
not clear whether the suppression of sex 2
hormones influences eating and/or exercise
habits. However, short-term hormone
suppression has been found to cause a decrease
in resting metabolic rate of 40 to 70 kcal per
day.4 This reduction in metabolic rate would be
expected to cause weight gain if not
accompanied by a compensatory decrease in
energy intake or increase in physical activity.

Aging-related factors that promote weight gain.
Even if the menopause transition does not alter
bioenergetics in a way that promotes weight
gain, there are unavoidable factors related to
aging that do so. Two important factors are the
loss of muscle mass and the decline in maximal
aerobic power. Lean body mass is an important
determinant of resting metabolic rate. As lean
mass declines with aging, there is a decrease in
metabolic rate and, therefore, daily energy
expenditure. The decline in metabolic rate will
result in weight gain unless appropriate
behavioral changes are adopted (ie, decrease in
energy intake or increase in physical activity).

Maximal aerobic power, also referred to as
aerobic capacity or VO2 max, is a direct index of
the rate at which an individual can expend
energy during exercise. For example, a healthy
young woman with an average VO2 max for her
age can easily increase her energy expenditure
by 8 to 10 kcal per minute during exercise.
However, there is a decline in VO2 max with
aging that cannot be avoided, due in part to the
inevitable decrease in maximal heart rate (ie,
maximal heart rate = 220 minus age).
Accordingly, with advancing age there is a
decline in the rate at which energy can be
expended during exercise, even in people who
maintain a vigorous level of physical activity.5
Rather than being able to increase energy
expenditure by 8 to 10 kcal per minute during
exercise, middle-aged women may be able to
burn only 6 to 8 kcal per minute. This has an
important impact on how women can use
exercise to maintain body weight as they age.
Because the rate at which energy can be
expended decreases gradually with aging,
maintaining the same level of total exercise
energy expenditure may require an increase in
the amount of exercise time.
Do physically active women gain less weight
than sedentary women during peri- and
postmenopause? Exercise can prevent weight
gain in peri- and postmenopausal women, but
factors related to menopause and aging make
weight maintenance a challenge. Even though
regular exercise does not come with a guarantee
against weight gain, prospective studies of
perimenopausal women indicate that the most
active women gain the least weight.6,7 Most
important, women should not abandon their
exercise habits if they become discouraged by
what they perceive as a lack of effectiveness of
exercise to prevent weight gain. Exercise has
numerous health benefits that are independent of
its effects on body weight regulation.8

Disclosure: Dr. Kohrt reports: Research support—
National Institutes of Health.

References:
1. Shi H, Clegg DJ. Sex differences in the regulation of
body weight. Physiol Behav 2009 Feb 27. [Epub ahead of
print]
2. Lobo RA. Metabolic syndrome after menopause and
the role of hormones. Maturitas 2008;60:10-18.
3. Yamasaki H, Douchi T, Yamamoto S, Oki T,
Kuwahata R, Nagata Y. Body fat distribution and body
composition during GnRH agonist therapy. Obstet
Gynecol 2001;97:338-342.
4. Day DS, Gozansky WS, Van Pelt RE, Schwartz RS,
Kohrt WM. Sex hormone suppression reduces resting
energy expenditure and beta-adrenergic support of resting
energy expenditure. J Clin Endocrinol Metab 2005;90:
3312-3317.
5. Hawkins SA, Marcell TJ, Victoria JS, Wiswell RA.
A longitudinal assessment of change in VO2 max and
maximal heart rate in master athletes. Med Sci Sports
Exerc 2001;33:1744-1750.
6. Sternfeld B, Wang H, Quesenberry CP Jr, et al.
Physical activity and changes in weight and waist
circumference in midlife women: findings from the Study
of Women’s Health Across the Nation. Am J Epidemiol
2004;160:912-922.
7. Macdonald HM, New SA, Campbell MK, Reid DM.
Longitudinal changes in weight in perimenopausal and
early postmenopausal women: effects of dietary energy
intake, energy expenditure, dietary calcium intake and
hormone replacement therapy. Int J Obes Relat Metab
Disord 2003;27:669-676.
8. Haskell WL, Lee IM, Pate RR, et al. Physical activity
and public health: updated recommendation for adults
from the American College of Sports Medicine and the
American Heart Association. Circulation 2007;116:1081-
1093.

Vulvodynia: Natural Approaches

This is a great intro to vulvodynia, which is a common syndrome affecting up to 15% of women and causing pain, burning or irritation of the vulva. Tori Hudson did a fine job in this essay, and rather than re-invent the wheel, I thought I'd post her work. -- SG

Vulvodynia: Diagnosis and Treatment

by Tori Hudson, ND

Vulvodynia or vulvar pain syndrome is a multifactoral clinical syndrome of vulvar pain, sexual dysfunction, and psychological distress. Recognizing the four specific subtypes of vulvodynia is important in the management approach. The most common four subtypes are vulvar vestibulitis syndrome, cyclic vulvovaginitis, dysesthetic vulvodynia, and vulvar dermatoses. Simple clinical guidelines can be developed to improve the evaluation and treatment of these often long-suffering patients.

Vulvodynia is different from itching or vulvar pruritus. Vulvodynia actually precludes itching because the burning and pain cause an intolerance to scratching. Over the years, the terminology used to describe vulvodynia has varied. The term vulvodynia has now been recommended by the International Society for the Study of Vulvar Disease (ISSVD) to describe any vulvar pain, regardless of etiology.

Vulvar pain usually has an acute onset. The onset can be associated with vaginitis (yeast, bacterial), changes in sexual activity (new sexual partner), or medical procedures on the vulva (cryotherapy, laser). In most cases, the vulvar pain then becomes a chronic problem varying in length from months to years. The intensity of the pain can vary from mild to disabling. It can be burning, stinging, irritating or raw. Most women with vulvodynia have been to many physicians either with inaccurate diagnoses or unsatisfactory treatment. Many women have been left feeling especially frustrated and at times mistreated because they have been told that their problem is purely psychological and there is nothing physically wrong with them. Because of the dramatic impact on their lives these women continue to seek help, and can become increasingly fearful and anxious about cancer or sexually transmitted diseases.

The incidence of vulvodynia is not known but it is clearly more common than is generally thought. In a general gynecological practice the prevalence can be as high as 15% when actively looked for.1 Characteristics of the patients with vulvodynia are nonspecific. The age distribution ranges from mid-20s to late 60s. Their Ob/Gyn history is unremarkable. They generally do not have other chronic health problems, and rarely have a history of sexually transmitted diseases. Sexual promiscuity is generally not a factor in these cases. Often, women with vulvodynia do report depression, but it is just as easily a result of the condition as it is a cause.

The pain reported can be in the general vulvar area, but is typically located in the vulvar vestibulum. The vestibule comprises the area between the labia minora and the hymenal ring, anteriorly from the frenulum of the clitoris, and posteriorly from the fourchette to the vaginal introitus. The urethra, Skenes glands, Bartholins glands and the minor vestibular glands are all located in the vulvar vestibule.

Only minimal findings are detected on the physical examination and most of the time there are not physical findings at all. The cotton tip applicator is used to determine the location of the pain. Touching the vestibulum lightly with a moist cotton-tipped swab reveals a sharp pain most often in the posterior vestibule, anterior vestibule or both. Occasionally red spots of inflammation can be detected at 5 oclock and 7 oclock or in a U-shaped area at the posterior fourchette.

Classification of Vulvodynia
Vulvar Dermatoses
Vulvar dermatoses can often cause both itching or pain and can be acute or chronic. Dermatoses are also dissimilar to other causes of vulvodynia because there can be physical signs of erythema, erosion or blisters. A partial list of vulvar dermatoses includes psoriasis, seborrheic dermatitis, tinea cruris, contact dermatitis, lichen simplex chronicus, lichen planus, lichen sclerosus, pemphigus, and erythema multiforme. Many dermatoses can be difficult to diagnose and may require a biopsy for a definitive diagnosis.

Cyclic Vulvovaginitis

Cyclic vulvovaginitis (CVV) is probably the most common cause of vulvodynia. The pain is typically cyclic and specifically worse during the luteal phase of the cycle. Symptoms are characteristically aggravated by vaginal sexual activity with the pain being usually worse the next day.2,3 CVV is thought to be caused by a hypersensitivity reaction to Candida antigen. If Candida cannot be detected during the symptomatic phase by culture, due to the bodys immune response, then culture specimens during an asymptomatic phase.

Conventional treatments include antimycotics for temporary relief, but symptoms recur soon after the treatment. Boric acid suppositories twice daily for 4 weeks and then once per day for 5 days during the menses only, for 4 more months is generally more successful for chronic yeast vaginitis than conventional antifungal agents. Boric acid suppositories were effective in curing 98% of the patients who had previously failed to respond to the most commonly used antifungal agents.4 However, many women do not tolerate the boric acid that leaks out of the vagina and further irritates the tissue. Lanolin or vitamin E oil or petroleum jelly or some other ointment (calendula) can be used to coat the vulvar tissue at the posterior fourchette where the irritation would be greatest. Other alternative treatments include local treatments such as lactobacillus suppositories, tea tree suppositories, garlic suppositories, herbal combination suppositories or douches (berberis hydrastis, usnea); systemic immune support (A, C, E, Zn, Glycyrrhiza glabra, Allium sativum, Hydrastis canadensis). Swabbing the vagina with genitian violet has been a longstanding specific treatment for candida, as has iodine douching (one part iodine in 100 parts water, twice daily for 14 days). Reinoculation from the anus requires attention to hygiene and possibly an approach that also addresses the gastrointestinal tract. Dietary considerations include a diet low in simple carbohydrates and refined foods, low in alcohol, and low in fats.

Vulvar Vestibulitis Syndrome
Vulvar vestibulitis syndrome (VVS) is characterized by dyspareunia, severe point tenderness on touch (positive cotton swab test), and erythema. The etiology of VVS is unknown. Some cases are aggravated by yeast vaginitis. Other suspected causes include chemical sensitivities, other irritants, a history of laser or cryotherapy, and allergic drug reactions. Some studies have suggested that VVS may be associated with human papillomavirus (HPV).5,6

Treatment of VVS is difficult and can require great patience and persistence on the part of both patient and practitioner. Conventional treatment is often fraught with overtreatment using antimicrobials and destructive or ablative therapies for suspected HPV. Conventional treatment can escalate to include interferon injections and vestibulectomy for severe incapacitating cases. The most promising alternative treatment that I have experienced in my practice is the use of calcium citrate. In patients whose urine shows evidence of excess oxalate, epithelial reactions similar to those found in vulvodynia are observed. Women have periodic hyperoxaluria and pH elevations related to the symptoms of vulvar pain. 1000mg of calcium citrate daily, in divided doses, is given to modify the oxalate crystalluria. A low oxalate diet is an additional cornerstone to managing these cases.7

In addition, I can cite cases in my private practice where an eclectic treatment plan of a topical ointment (vitamin A, tincture of thuja and lomatium isolate), oral beta carotene (75,000IU to 150,000/day), eliminating food intolerances, and a constitutional homeopathic remedy, have yielded anywhere from 50% improvement to 100% improvement. Unfortunately, I can also cite cases where there was only minimal improvement. I have heard anecdotal reports using elaborate chemical desensitizing methods and dramatic improvements, but I have not personally investigated these cases. Psychological intervention must always be considered for assistance in dealing with the illness, and perhaps therapeutic intervention can then allow the immune system to adequately address the chronic syndrome.

Dysesthetic Vulvodynia
This subtype of vulvodynia is more common among older women who are either perimenopausal or postmenopausal. Patients have constant noncyclic vulvar or perineal discomfort. These women have less dyspareunia and less point tenderness than the women with VVS. No significant changes are observed on the physical examination except diffuse hyperaesthesia which occurs on a wider area compared to VVS. Sharp pain can also be elicited with light touch. The hyperaesthesia is thought to be a result of an altered sense of cutaneous perception. A neurological basis is probably the explanation for the nonspecific burning. The sensation mimics the neuralgia associated with herpes. Urethral or rectal discomfort is often associated with their vulvar pain.

Conventional medicine often prescribes tricyclic antidepressants8 for dysesthetic vulvodynia. Side effects are a common problem with tricyclics, and occur in up to half of the patients. Theoretical nutritional and botanical alternatives for dysesthetic vulvodynia include Folic acid, B12, Piper methysticum (kava-kava), Ginkgo biloba, Hypericum perforatum (St. Johns Wort).

Physical Therapy for Vulvar Pain
The use of physical therapy to relieve vulvar pain should not be overlooked. Spasm of the inner thigh muscles or hip muscles can be a result of guarding against the pain of weight resting directly on vulvar skin while sitting. There are specific devices for removing pressure from the vulvar area when sitting. Manual therapy techniques can also be used to relieve pain by releasing severe muscle spasms. Trigger points in the pelvic floor muscles from fibromyalgia can refer pain to the vulvar skin and the vagina. Trigger point therapy and pelvic floor muscle strengthening and relaxation can also relieve pelvic floor muscle spasms.

Vulvar pain syndromes provoke psychological as well as physical distress. Sexual relationships become seriously strained in women with vulvodynia. Women tend to feel defective, less womanly, less sexually attractive ashamed and embarrassed. Dealing with spouses and partners who are having difficulty coping is an additional stress. Anxiety and depression set in with unsatisfactory visits to their health care practitioners and unsatisfactory results. Hopelessness can become the greater illness but practitioners should be cautioned against being overly optimistic in encouraging them to try another promising treatment. If it fails, it further escalates the hopelessness.

Knowledge of the specific subsets of vulvodynia is extremely important in improving the diagnosis and treatment of this complex multifactoral syndrome. Simple guidelines and recommendations augment the evaluation and management.9

Rule out underlying problems
Biopsy suspicious lesions
Do not overlook cervix
Use a multidisciplinary approach
Differential diagnosis of vulvar dermatoses
Differential diagnosis of vulvar erosions
Provide empathy and support
Educate the patient in their understanding of the problem
Help the patient to cope with the problem
Inform them that symptoms fluctuate
Best questions to be asked
Are there any days without burning?
Is the pain related to menses?
How is the pain associated with vaginal penetration?
Set simple goals
Less bad days, more good days
Getting better takes some time
Coach them to stick with the treatment

References

1. Goetsch MF. Vulvar vestibulitis: Prevalence and historic features in a general gynecologic practice population. Am J Obstet Gynecol 1991; 164:1609-16.

2. McKay M. Vulvodynia: a multifactorial clinical problem. Arch Dermatol 1989; 125.

3. McKay M. Subsets of vulvodynia. J Reprod Med 1988; 33:695-8.

4. Jovanovic R, Congema E, Nguyen H. Antifungal Agents vs. Boric Acid for Treating Chronic Mycotic Vulvovaginitis J Reprod Med 199;36:593-597.

5. Turner MLC, Marinoff SC. Association of human papillomavirus with vulvodynia and the vulvar vestibulitis syndrome. J Reprod Med 1988; 33:533-7.

6. Umpierre SA, Kaufman RH, Adam E, Woods KV, Adler-Storz K. Human papillomavirus DNA in tissue biopsy specimens of vulvar vestibulitis patients treated with interferon. Obstet Gynecol 1991; 78:693-5.

7. Sollomons C, Melmed M, Heitler S. Calcium Citrate for Vulvar Vestibulitis. J Reprod Med 1991; 36:879-882.

8. McKay M. Dysesthetic (essential) vulvodynia. Treatment with amitriptyline. J Reprod Med 1993; 38:9-13.

9. Paavonen J. Diagnosis and Treatment of Vulvodynia. Ann Med 27:175-181, 1995. Resources The Vulvar Pain Foundation, P.O. Drawer 177, Graham, North Carolina 27253; 910-226-0704.