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Lynch syndrome explainer: a common cancer risk few have heard of

Lynch syndrome explainer: a common cancer risk few have heard of

March 25, 2016 7.51am AEDT

When the DNA repair tool is faulty or broken, cancer happens. from http://www.shutterstock.com.au

Lynch syndrome is the most prevalent inherited cancer syndrome affecting both men and women. It is caused by an inherited gene mutation affecting one of four mismatch repair or “cancer protection” genes (MLH1, MSH2, MSH6, PMS2).

Mismatch repair genes should repair mistakes that can occur when DNA is copied for cell division. Faulty mismatch repair genes allow errors to accumulate in cells, which can lead to uncontrolled cell growth and cancer.

Up to one in 250 people may carry a mismatch repair gene fault. As many as one in 280 carry a fault in a Lynch syndrome gene.

A parent with Lynch syndrome has a 50% chance of passing on the faulty gene to their children, regardless of gender. However, because a carrier inherits one faulty gene and one properly functioning gene, some people with Lynch syndrome may never develop cancer.

Lynch syndrome does not cause cancer and has no readily identified symptoms, but the faulty gene predisposes carriers to a dramatically increased risk of developing one or more primary cancers over their lifetime. As this tool shows, the risk varies by type of tumour, age, gender and the particular mismatch repair gene that is affected. In people with the syndrome, cancers are often fast growing, may occur simultaneously and tend to occur from a much younger age (under 50 and sometimes in the 20s or earlier).

If an individual knows they have Lynch syndrome, they can adopt life-saving strategies for cancer prevention, early detection and treatment.

Lynch syndrome awareness video

What cancers are associated with Lynch syndrome?

Patterns of Lynch syndrome cancers in families were first observed by Dr Aldred Warthin in the 1890s. However, the condition is named after Dr Henry Lynch, who persisted against the prevailing wisdom of the 1960s-70s – which disputed a hereditary basis for cancer – to document, describe and establish the genetic basis for Lynch syndrome.

For a time, Lynch syndrome was called hereditary non-polyposis colon cancer. That was an unfortunate misnomer because Lynch syndrome cancers can involve polyps and don’t just involve colon cancers.

Lynch syndrome is most commonly associated with colorectal and endometrial cancers. It also significantly increases the risk of cancer of the ovary, stomach, hepatobiliary tract (liver/gallbladder), urinary tract, pancreas, brain, skin, oesophagus and small bowel.

Some tumours may also present differently in individuals with Lynch syndrome. Examples include the unusually flat, difficult-to-detect polyps and tumours sometimes observed in bowel and breast cancers.

How is Lynch syndrome diagnosed?

GPs should suspect an individual may carry a Lynch syndrome gene when there is a compelling family history of cancer. This means three or more family members have been diagnosed with cancers identified above, two consecutive generations or more are affected by those cancers, and one of those affected family members was diagnosed with cancer before 50 years of age. It should also be suspected where a patient has little or no access to their family’s health history information and has already had one or more relevant cancers before age 50.

Family history of cancer as above could signify Lynch syndrome. Source: Lynch syndrome Australia.

If Lynch syndrome is not identified and the patient develops cancer, they will typically require surgery to remove the tumour. Current best practice for all colon and endometrial tumours for patients under age 50, or who have a strong family cancer history, is for the treating team to order a pathology test to check mismatch repair genes are functioning properly.

Unfortunately, research reveals less than half of these tumours are tested and patient follow-up is confusing and inconsistent.

Any patient suspected of carrying Lynch syndrome should be referred to a family cancer clinic. There, a genetic counsellor will conduct a thorough assessment and explain the gene-testing process and its implications. With patient consent, the clinic will arrange testing of a tissue sample from a past tumour (either the patient’s or another family member’s) to search for a mismatch repair gene mutation.

If a gene mutation is detected, risk-reducing strategies are discussed. Diagnosis for other family members then involves a relatively simple blood test, which looks for the same mutation.

How is Lynch syndrome managed?

Managing Lynch syndrome involves a surveillance plan of regular tests to detect problems early. Then polyps can be removed before they become cancerous or cancers can be removed at an early stage. The potential for risk-reducing surgery (to remove organs, such as ovaries, that are high risk yet difficult to screen) or supplements such as aspirin (which longitudinal studies suggest may significantly reduce the incidence of Lynch syndrome cancer) may also be considered.

Guidelines recommend annual colonoscopies (from age 25 or 30, depending on the gene mutation, or five years younger than youngest relative diagnosed with bowel cancer) and prophylactic removal of the uterus, fallopian tubes, ovaries and cervix be considered after childbearing is complete, or by age 40.

Frequent colonoscopies are important because the average time from polyp to bowel cancer reduces from ten years in the general population to just 35 months in patients with Lynch syndrome. Similarly, the average age for developing uterine cancer reduces from 64 years to 42-46 years.

An individual’s surveillance plan may be further tailored to address specific cancer risks for them, based on family history or environmental factors. For example, a family history of gastric or skin cancers may justify including annual endoscopy or dermatological reviews.

Effective diagnosis and management of individuals with Lynch syndrome can be life-saving. Unfortunately, this is not the experience for thousands of Australian families. It’s important we raise awareness of this condition among medical professionals, health organisations and the general public.

Tobacco exposure negatively impacts womens reproductive health

Tobacco exposure negatively impacts womens reproductive health

Roswell Park Cancer Institute News, 01/20/2016

The risk of infertility and early menopause increases significantly for women who use tobacco or are exposed to secondhand smoke, according to a study led by Roswell Park researchers and published in the current issue of Tobacco Control. Information about smoking, lifetime fertility status and age of menopause was analyzed from 88,732 women who participated in the Women’s Health Initiative Observation Study. This is one of the first studies of this size and statistical power to investigate and quantify the impact of active tobacco use and exposure to secondhand smoke on women’s reproductive health. “This study strengthens current evidence that all women need to be protected from active and passive tobacco smoke,” said Andrew Hyland, PhD, Chair of the Department of Health Behavior at Roswell Park. “The toxins found in tobacco smoke are known to adversely impact both fertility and the natural age of menopause. Smoking negatively impacts every organ in every part of the body.” One noteworthy finding of this study is the impact of secondhand smoke on nonsmokers. Exposure to secondhand smoke as a child, living 20 or more years with someone who smoked at home, or working for 10 or more years with colleagues who smoked increased a woman’s risk of infertility problems by 18%. These women also underwent menopause an average of 13 months earlier than lifetime nonsmokers. Early menopause is associated with premature death. Current or former women smokers experienced menopause 1 to 2 years earlier than lifetime nonsmokers. Tobacco use also increased their risk for menopause before age 50 by 26%. These smokers also had a 14% increased risk of infertility. The study was published in the journal of Tobacco Control

Coffee, Caffeine and Hypertension Risk

Coffee, Caffeine and Hypertension Risk

A study in postmenopausal women

December 22, 2015

Caffeinated coffee, decaffeinated coffee, and caffeine are not risk factors for hypertension in postmenopausal women, according to a study of 29,985 postmenopausal women who were not hypertensive at baseline. During 112,935 person-years of follow-up, 5,566 cases of incident hypertension were reported. The study also found:

• Neither caffeinated coffee nor caffeine intake was associated with mean systolic or diastolic blood pressure.

• Decaffeinated coffee intake was associated with a small but clinically irrelevant decrease in mean diastolic blood pressure.

• Decaffeinated coffee intake was not associated with mean systolic blood pressure.

• Intakes of caffeinated coffee, decaffeinated coffee, and caffeine were not associated with the risk of incident hypertension.

Citation: Rhee JJ, Qin F, Hedlin H, et al. Coffee and caffeine consumption and the risk of hypertension in postmenopausal women. [Published online ahead of print December 9, 2015]. Am J Clin Nutr. doi: 10.3945/​ajcn.115.120147.

Commentary: This study presents further data to reassure us about our favorite stimulant – coffee. Coffee consumption has also been shown to be associated with a decreased risk of type 2 diabetes, Parkinson’s disease, and fatal prostate cancer.1  In addition, a recent article with over 4 million person-years of observations showed that compared to non-drinkers, coffee consumption of 1 to 5 cups/day was associated with lower mortality.2  —Neil Skolnik, MD

1.  Ding M, Bhupathiraju SN, Chen M, van Dam RM, Hu FB. Caffeinated and decaffeinated coffee consumption and risk of type 2 diabetes: A systematic review and a dose-response meta- analysis. Diabetes Care. 2014;37:569-586.

2.  Ding M, Satija A, Bhupathiraju SN, et al. Association of coffee consumption with total and cause-specific mortality in 3 large prospective cohorts.  Circulation. 2015;132(24):2305-2315. doi: 10.1161/CIRCULATIONAHA.115.017341.

Kitchen Science: from sizzling brisket to fresh baked bread, the chemical reaction that makes our favourite foods taste so good

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Kitchen Science: from sizzling brisket to fresh baked bread, the chemical reaction that makes our favourite foods taste so good

June 3, 2016 6.23am AEST

Disclosure statement

Les Copeland does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond the academic appointment above.

 

Have you ever wondered how freshly baked bread gets its a golden brown crust and why it smells so good? Or how nondescript green berries turn into beautiful brown coffee beans with a rich alluring aroma?

The answers to these questions lie in a series of complex of chemical reactions, known as Maillard reactions, which give many foods their familiar flavours and colours. These sensory properties even guide us in how we choose foods and help create our initial perceptions of their quality.

As the name suggests, Maillard reactions were first described by a French physician and biochemist, Louis-Camille Maillard, in 1912. These reactions produce hundreds of chemical compounds that give colour and aroma to some of our favourite foods such as roast meat, potato chips, bread and other bakery products, coffee, chocolate and confectionery.

Maillard reactions occur between amine groups of amino acids or proteins and “reducing” sugars, such as glucose and fructose. These sugars are so named because they act as chemical reducing agents.

These reactions occur most rapidly under conditions of low moisture and at temperatures above about 130℃. Hence, they tend to kick in when we fry, bake, grill or roast.

Maillard reactions are also referred to as browning reactions because of the colour they impart to foods cooked in this way. When meat is grilled or roasted, only the surface is usually hot enough to cause browning. The interior can retain a pinkish colour because the cooking temperature stays below that required for Maillard reactions to occur rapidly.

Foods cooked by boiling or steaming do not turn brown or acquire the complexity of flavours because the temperature only reaches about 100℃. Likewise with cooking in a microwave oven.

The colour of chocolates, fudges and toffees are produced by the reaction of sugars with milk proteins.

The initial products of Maillard reactions are small volatile molecules, which are responsible for the aromas we get from freshly baked bread and coffee. More complex reactions then take place to form larger molecules responsible for the golden to brown colours. This is why the aroma of baking bread is sensed before the crust browns.

The later Maillard reactions are not well understood. We do know that some of the molecules they form have unpleasant flavours and may even be toxic, or the source of carcinogens that occur in charred meat.

The Maillard reaction not only turns it golden brown, but also releases mouth watering aromas. Shutterstock

The colour of flavour

A common misconception is that Maillard reactions are the same as caramelisation. Although both are favoured by conditions of low moisture, caramelisation occurs when sugars are heated to high temperatures in the absence of proteins. The common food flavour and caramel colour is produced by heating a mixture of glucose and sucrose to 160℃.

Maillard reactions don’t only take place in a hot oven though. They can also occur slowly at ambient temperature, resulting in gradual changes to aroma, flavour, colour, appearance, texture, shelf-life and nutritional value of stored foods.

In this way, Maillard reactions are responsible for the colour of honey, as well as deterioration during storage of dry goods such as flour and powdered milk. Maillard reactions are also implicated in the gradual loss of viability of seeds.

Maillard reactions can also have detrimental consequences. Unsightly blemishes may appear on chips after frying if their reducing sugar content exceeds 0.03% of dry matter. Potatoes destined for commercial chip production are carefully monitored to ensure reducing sugars are below this level.

An undesirable product of Maillard chemistry is acrylamide. This is a chemical that can be detected in tiny amounts in a range of fried or roasted foods, including potato chips, coffee, cocoa, chocolate and cereal-based bakery products, sweet biscuits and toasted bread (but not in steamed buns).

Acrylamide has been mentioned as a possible carcinogen, although according to Food Standards of Australia and New Zealand, the body that oversees the safety of our food, there is no direct evidence it causes cancer in humans. Acrylamide does not occur in raw foods or foods cooked by boiling or steaming.

You can almost smell it from here. THINK Global School, CC BY-NC-ND

Beyond the kitchen

Some aspects of the Maillard reaction have long been implicated in human ageing and health conditions.

Examples include loss of elasticity of connective tissue and the appearance dark spots on skin due to effects on collagen, cataract formation due to reactions with the lens protein crystallin, changes in neural proteins contributing to neuropathology and dementia, and glycation of haemoglobin due to elevated blood glucose levels in diabetes.

The importance of Maillard reactions in the kitchen and beyond is well established, even though these reactions are still not well understood more than a century after they were first described.

Nevertheless, we can take advantage of their benefits while continuing to learn about this fascinating area of chemistry

Cholesterol lowering tablets (Statins) in the over 65s.

Many of my older patients have been given cholesterol lowering drugs – the evidence is against their use in older women and the side effects make them unacceptable. Be aware of the evidence as some doctors are too hasty to dish out cholesterol(statins) tabs to their older patients
JAMA Intern Med. 2017 Jul 1;177(7):955-965. doi: 10.1001/jamainternmed.2017.1442.

Effect of Statin Treatment vs Usual Care on Primary Cardiovascular Prevention Among Older Adults: The ALLHAT-LLT Randomized Clinical Trial.

Author information

1
Division of Geriatric Medicine and Palliative Care, Department of Medicine, New York University School of Medicine, New York.
2
Section on Gerontology and Geriatric Medicine, Department of Internal Medicine, Wake Forest School of Medicine, Winston Salem, North Carolina.
3
Coordinating Center for Clinical Trials, University of Texas School of Public Health, Houston.

Abstract

Importance:

While statin therapy for primary cardiovascular prevention has been associated with reductions in cardiovascular morbidity, the effect on all-cause mortality has been variable. There is little evidence to guide the use of statins for primary prevention in adults 75 years and older.

Objectives:

To examine statin treatment among adults aged 65 to 74 years and 75 years and older when used for primary prevention in the Lipid-Lowering Trial (LLT) component of the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT-LLT).

Design, Setting, and Participants:

Post hoc secondary data analyses were conducted of participants 65 years and older without evidence of atherosclerotic cardiovascular disease; 2867 ambulatory adults with hypertension and without baseline atherosclerotic cardiovascular disease were included. The ALLHAT-LLT was conducted from February 1994 to March 2002 at 513 clinical sites.

Interventions:

Pravastatin sodium (40 mg/d) vs usual care (UC).

Main Outcomes and Measures:

The primary outcome in the ALLHAT-LLT was all-cause mortality. Secondary outcomes included cause-specific mortality and nonfatal myocardial infarction or fatal coronary heart disease combined (coronary heart disease events).

Results:

There were 1467 participants (mean [SD] age, 71.3 [5.2] years) in the pravastatin group (48.0% [n = 704] female) and 1400 participants (mean [SD] age, 71.2 [5.2] years) in the UC group (50.8% [n = 711] female). The baseline mean (SD) low-density lipoprotein cholesterol levels were 147.7 (19.8) mg/dL in the pravastatin group and 147.6 (19.4) mg/dL in the UC group; by year 6, the mean (SD) low-density lipoprotein cholesterol levels were 109.1 (35.4) mg/dL in the pravastatin group and 128.8 (27.5) mg/dL in the UC group. At year 6, of the participants assigned to pravastatin, 42 of 253 (16.6%) were not taking any statin; 71.0% in the UC group were not taking any statin. The hazard ratios for all-cause mortality in the pravastatin group vs the UC group were 1.18 (95% CI, 0.97-1.42; P = .09) for all adults 65 years and older, 1.08 (95% CI, 0.85-1.37; P = .55) for adults aged 65 to 74 years, and 1.34 (95% CI, 0.98-1.84; P = .07) for adults 75 years and older. Coronary heart disease event rates were not significantly different among the groups. In multivariable regression, the results remained nonsignificant, and there was no significant interaction between treatment group and age.

Conclusions and Relevance:

No benefit was found when pravastatin was given for primary prevention to older adults with moderate hyperlipidemia and hypertension, and a nonsignificant direction toward increased all-cause mortality with pravastatin was observed among adults 75 years and older.

Hormones and Sarcopenia

As most of us get older, we will all develop sarcopenia (frailty) to some degree.  Hormones, especially testosterone, are vitally important in helping to offset this process. 

Curr Pharm Des. 2017 Apr 28. [Epub ahead of print]

Hormones and Sarcopenia

Author information

1
Division of Geriatric Medicine, Director, Saint Louis University School of Medicine, St. Louis, Missouri USA.

Abstract

Sarcopenia is defined as the loss of muscle mass associated with a loss of muscle function, e.g., walking speed. A number of consensus definitions exist for sarcopenia with cut-off points being ethnically specific. A rapid screen test (SARC-F) is available and does not require different ethnic cut-off points. Sarcopenia leads to the development of frailty, disability and mortality. The prevalence of sarcopenia varies from 1-29% in community-dwelling and 14 to 33% in long-term care populations. Hormones play a role in the development of muscle mass and in the regulation of muscle strength. Testosterone appears to be the central hormone involved in the development of sarcopenia; it increases both muscle mass and activates satellite cells leading to increased muscle function. Growth hormone deficiency leads to the loss of muscle mass but not muscle strength. Lack of insulin or insulin resistance leads to accelerated development of sarcopenia. Vitamin D deficiency plays a role in the loss of muscle strength. A variety of other hormones appear to play minor roles in age-related alterations in muscle mass and function. At present, the treatment of sarcopenia is resistance exercise, leucine enriched essential amino acids or hydroxymethylbutyrate and vitamin D replacement

what is eczema and what can you do about it?

Explainer: what is eczema and what can you do about it?

 

Eczema is a genetic disorder with an environmental trigger, which affects one in three people at some time in their life..

People with eczema essentially have sensitive skin that is easily irritated. The irritation produces dryness by disrupting the function of the external waterproof skin barrier, allowing water to leave the skin.

The main gene associated with eczema – or atopic dermatitis, as it’s known clinically – is filaggrin. Filaggrin mutations reduce the ability of the skin to withstand environmental insults and to repair itself after injury.

Disruption to the skin barrier allows allergens to enter the deeper layers of the skin and activate the immune system.

How the immune system reacts to these allergens determines the severity of the skin inflammation and the duration of the disruption to the skin barrier function.

What can you do about it?

If you or someone in your family has suffered with severe eczema, you’ve probably tried all sorts of remedies to alleviate the itching. Here are five tips to calm your skin:

1) Avoid things that irritate the skin. No matter how wonderful a hot shower feels on itchy skin, it actually aggravates eczema. Keep showers to five minutes or less and use luke-warm water.

Wash with water alone: no soap, no soap substitute, no soap-free wash and definitely no bubble bath. Just water.

2) Avoid overheating. Heat makes the itch worse, irrespective of the cause. Turn the heating down to 18 to 20 degrees Celsius (64 to 68 degrees Farenheit) and put on an extra layer of clothing.

Take the doona off your bed and sleep under good old-fashioned cotton blankets. Overheating at night leads to scratching in your sleep. If there is blood on your sheets in the morning, that is a sure sign your bed is too hot at night.

Apply moisturiser frequently and liberally. Kaspars Grinvalds/Shutterstock.
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3) Take a bleach bath. This is a simple method to reduce the bacteria on the surface of your skin. For a full tub of water, use half a cup of bleach. Never apply bleach directly to the skin. (More safety tips and instructions are available here.)

If the eczema is weeping, oozing or has honey-coloured crusts, there is almost always golden staph on the skin surface aggravating the eczema. Bleach baths are a good alternative to antibiotics.

4) Use lots and lots of moisturiser. To fix eczema you will also need to restore the skin barrier. That requires frequent and liberal use of moisturiser, including after the eczema appears to have cleared up.

There are lots of moisturisers on the market. Trial and error is the best way to find the right moisturiser for your skin. Keep in mind that if you use a light one, you need to reapply it more often than a heavy one.

While tablets can help stop the inflammation, in general that’s not enough to stop the eczema.

5) Use your topical corticosteroid creams as directed. Additives reduce the skin thinning that can occur with prolonged use of potent topical steroids. Your dermatologist is the best person to advise you on this.

Emerging therapies

Researchers are investigating whether a new class of drugs, called biologics, could help manage severe eczema.

Biologics show promise but they’re still several years away. Quayside/Shutterstock

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Biologics try to block critical steps within certain pathways, which can terminate inflammation.

Biologics are most commonly produced from bacteria or yeast cultures. Specific genes are inserted into bacteria and yeast that have been inactivated so they are no longer dangerous to humans.

Production of biologics in this way is slow, low-volume, high-tech and expensive. Consequently, biologics can cost tens of thousands of dollars per patient per year.

A number of clinical research trials are underway to test these agents. People with severe eczema, which is not adequately controlled with current treatments, may consider enrolling to participate in a research trial.

It will still take three to five years for the results of these trials to be fully assessed and to know whether biologic agents are safe and effective in the management of eczema. If they are, they could revolutionise the management of severe eczema.

Why we regain weight after drastic dieting

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Why we regain weight after drastic dieting

June 21, 2016 6.13am AEST

Disclosure statement

Sergio Diez Alvarez does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond the academic appointment above.

Partners

University of Newcastle provides funding as a member of The Conversation AU.

 

A few years ago I proudly lost almost 15% of my weight. However last week I stared with disbelief at my scale as I realised all my efforts were in vain and I had regained all of the previously lost weight.

This got me thinking about the mechanisms that underpin such dramatic fluctuations in weight (sometimes known as yo-yo dieting) and the defences the body uses for weight maintenance.

Even losing as little as 5% of our body weight has a myriad of health benefits, including reduced risk of heart attacks, lower blood pressure, improved glucose control in patients with diabetes, improved mental health and reduced risk of osteoarthritis and certain cancers.

Thus one would imagine the body would generally be supportive of weight loss. If so, why is persistent weight loss and weight maintenance so difficult?

Why the body fights weight loss

The control of weight is based on the balance between calorie consumption and the energy spent during our day to day living. The brain’s weight control centre is in an area called the hypothalamus.

The hypothalamus integrates the incoming signals from the body (such as hormonal signals) and other parts of the brain and then controls weight by affecting hunger and satiety.

It also communicates with other parts of the brain that control metabolism (such as the pituitary gland and sympathetic nervous systems). This complicated and fine-tuned system determines a “weight set-point” which is the weight the body is accustomed to and then works to defend it by fine tuning our metabolism and our calorie consumption.

Energy consumption is divided into the resting metabolic rate (about 70% of all energy used), the energy consumed in processing the food we eat (thermogenic metabolism) and exercise based energy expenditure.

A few studies have outlined the result of moderate weight loss. The body defends against weight loss by drastically reducing the energy expenditure. The body also goes into a sort of “starvation mode” to protect against lean body weight loss by preferentially depleting different energy stores including glycogen, fat and then eventually muscle.

The body spends a large percentage of energy in the maintenance of organ function, even when asleep. In obese people, the resting metabolic rate significantly increases, perhaps to try to prevent further weight gain. Unfortunately, when you lose weight, the opposite happens and the body’s metabolism turns right down.

This may occur through reductions in the active thyroid hormone (T3) and changes in the hormonal messages back to the brain promoting hunger.

A key finding in the above studies is the reduction in resting metabolic rate is disproportionately large, and potentially persists for long periods. This explains why a return to a pre-weight loss lifestyle inevitably results in weight re-gain, and possibly more than was lost.

Only by maintaining a healthy lifestyle with calorie restriction of around 25% and exercise can we avoid the inevitable. The reduction in resting metabolic rate may be particularly problematic in people with severe obesity.

Drastic long-term weight loss

This led me to examine the published data on contestants with severe obesity in The Biggest Loser. I wondered what had become of the contestants who had lost amazing amounts of weight over a relatively short period of time.

Majority of The Biggest Loser contestants regained a significant proportion of their lost weight. AAP Image/Channel Ten

One study confirmed that despite the rigorous exercise programs, the drop in resting metabolic rate persisted. In a study published this year that followed 14 of the original 16 contestants, the majority had regained a significant proportion of the weight loss. More importantly, their resting metabolic rate was still low, almost six years after the end of the show. This suggests the metabolic adaptation against rapid weight loss may be profound and sustained, possibly explaining why we potentially regain even more weight than we originally lost.

This same phenomenon was found after weight loss following a type of bariatric surgery, where weight loss is achieved by reducing the size of the stomach with a gastric band. The metabolic adaptation in these patients was very similar to that found with similar weight loss in The Biggest Loser.

The long-term data for bariatric surgery in terms of sustainability of weight loss suggests other factors (most likely related to gut hormones such as ghrelin) must be influencing energy balance as there is evidence that weight loss is maintained even after many years.

How to avoid the slowed metabolism

So is there a way to counter nature’s opposition to weight loss? Certain types of exercise such as strength exercises preserve muscle mass and this assists in preserving the resting metabolic rate. However it doesn’t always work.

Thus it may be that only sustained modest exercise and a permanent reduction in calories are both essential for weight loss and maintenance. Although there is no data on the rate of weight loss at which metabolic adaptation occurs, most guidelines recommend gradual and steady weight loss of between 0.5-1kg per week, as part of a sustainable lifestyle change which includes appropriate exercise activity and a balanced nutritious diet.

Is Hormone Replacement Therapy Safe in Women With a BRCA Mutation?

I have had many women concerned that they cannot have HRT due to being BRAC +ve, so they have had to suffer needlessly from the symptoms of menopause. This study can allay their fears
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Am J Clin Oncol. 2016 Feb 2. [Epub ahead of print]

Is Hormone Replacement Therapy Safe in Women With a BRCA Mutation?: A Systematic Review of the Contemporary Literature.

Abstract

OBJECTIVES:

Women with a BRCA1 or BRCA2 mutation are recommended to undergo prophylactic (or risk reducing) bilateral salpingo-oophorectomy (BSO) before age 40, resulting in surgical menopause. Given the concerns of estrogen deprivation on overall health, hormone therapy (HT) is often discussed, yet safety concerns persist.

MATERIALS AND METHODS:

We performed a systematic literature review of the safety of HT in women with a BRCA mutation undergoing prophylactic BSO.

RESULTS:

Although there remains a paucity of data on this topic, as evidenced by this systematic review of the contemporary literature, these patients do benefit from treatment, especially as it relates to menopausal symptoms without an apparently increased risk of breast cancer.

CONCLUSIONS:

Decisions regarding the use of HT in women who undergo BSO after detection of a BRCA mutation must be individualized based on careful consideration of the risks and benefits. However, the risks of a subsequent cancer diagnosis appear small, particularly in regards to the benefits of treatment afforded by HT

The effects of DHEA (dehydroepiandrosterone) on sexual function

Climacteric. 2017 Jan 24:1-12. doi: 10.1080/13697137.2017.1279141. [Epub ahead of print]

The effects of dehydroepiandrosterone on sexual function: a systematic review.

Author information

  • 1a Federal University of Rio de Janeiro, Institute of Psychiatry, Laboratory of Panic and Respiration , Rio de Janeiro , RJ , Brazil.
  • 2b Federal University of Rio de Janeiro, Institute of Psychiatry, Laboratory of Thanatology and Psychiatry in other Medical Conditions , Rio de Janeiro , RJ , Brazil.
  • 3c Translational Research Group in Mental Health , Dom Bosco Catholic University , Campo Grande , MS , Brazil.

Abstract

OBJECTIVE:

Faced with the growing interest about the action of dehydroepiandrosterone (DHEA) and its benefits, as well as the negative impacts that sexual dysfunctions have on people’s quality of life, this systematic review was undertaken with the objective of evaluating the effect of DHEA use on aspects of sexual function.

METHOD:

An electronic search was conducted in the databases of PubMed, ISI Web of Science and Virtual Health Library (VHL) combining the terms ‘DHEA treatment’ and ‘DHEA use’ with terms such as ‘sexual dysfunction’, ‘sexual frequency’ and ‘libido’. No limits on time and language were imposed. Clinical studies were considered eligible where individuals for any reason made use of DHEA and if they had any aspect of sexual function assessed. Preclinical studies and systematic reviews were considered ineligible.

RESULTS:

The search identified 183 references and 38 were considered eligible. DHEA improved aspects such as sexual interest, lubrication, pain, arousal, orgasm and sexual frequency. Its effect was better in populations with sexual dysfunction, especially in perimenopausal and postmenopausal women.

CONCLUSION:

Considering the studies currently published, DHEA is effective in improving several aspects of sexual function, but this effect did not reach all the populations studied.