Monthly Archives: October 2017

Cardiovascular disease in women, is it different to men? The role of sex hormones.

Climacteric. 2017 Apr;20(2):125-128. doi: 10.1080/13697137.2017.1291780. Epub 2017 Mar 2.

Cardiovascular disease in women, is it different to men? The role of sex hormones.

Author information

a Department of Cardiovascular and Cell Science Research , St George’s Hospital , London , UK.
b Department of Medical Sciences , IRCCS San Raffaele Pisana , Rome , Italy.


Cardiovascular disease in women differs in clinical presentation, pathophysiology and prognosis from that in men. The role of estrogens and androgens may help explain such sex dimorphisms, being involved in cardiac function, endothelial function and vascular tone. In particular, the cardioprotective effect of estrogen replacement therapy is observed in postmenopausal women in a time-dependent manner, i.e. when it is initiated at their first menopausal symptoms. Postmenopausal women, beyond aged men, may also benefit from testosterone supplementation therapy. Testosterone has been found to be an effective and safe therapy for elderly women with chronic heart failure. However, further studies are needed to clarify doses and routes of administration of androgens in postmenopausal women.

The effects of dehydroepiandrosterone on sexual function.

Climacteric. 2017 Apr;20(2):129-137. doi: 10.1080/13697137.2017.1279141. Epub 2017 Jan 24.

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

Author information

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



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.


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.


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.


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.

How do I know if I drink too much?


Health Check: how do I know if I drink too much?

September 19, 2016 2.36pm AEST

Disclosure statement

Bosco Rowland 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.


Victoria State Government provides funding as a strategic partner of The Conversation AU.

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

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While alcohol is a legal and common way many societies stimulate social interaction, when consumed at high levels over long periods it can undermine physical health and cause cancers and other disease. Most people know excessive drinking isn’t good for our health, but how do we know when we’re drinking too much?

Alcohol consumption is associated with long- and short-term consequences. Long-term health consequences include: alcohol-related diseases such as cirrhosis of the liver; stroke; high blood pressure; heart disease; and more than 60 cancers, including of the mouth, lips, throat, oesophagus, stomach, pancreas, liver, bowel and breast.

Short-term health consequences include fatalities, physical injury or road accidents due to impaired cognitive performance and diminished reaction times.

Social consequences may include domestic violence, absenteeism, violence and crime.

How much is safe to drink?

It’s important to know the recommendations on drinking to ensure we’re not drinking too much for our own health and for the safety of others.

In 2009, the National Health and Medical Research Council updated the Australian drinking guidelines. The guidelines contain four recommendations to ensure our drinking is “low risk”. Low risk is defined as drinking at a level that reduces the chance an individual will suffer from short-term injury or long-term disease.

Healthy men and women are advised not to drink more than two standard drinks on any one day. If a person drinks less than that, the probability he or she will suffer from long-term alcohol-related disease (such as cancer) is approximately one in 100.

For both men and women, drinking no more than four standard drinks on a single occasion reduces the risk of alcohol-related injury to one in 100. Risk of injury includes physical injury, or road accidents due to impaired cognitive performance and diminished reaction times.

Short-term risky drinking is most often associated with intoxication. Intoxication in its mildest form produces slight changes in inhibition, reduced co-ordination and decreased alertness. More extreme forms may involve slurred speech, boisterous or aggressive behaviour, inappropriate sexual behaviour, swaying, rambling conversation and difficulty concentrating.

Who can drink?

Pregnant women are advised to avoid alcohol because of the possibility of alcohol passing through the placenta into the embryo. This may affect brain and other developments of the child.

Evidence shows the brains of children under the age of 18 are still developing. Thus it is recommended children under the age of 18 should avoid consuming alcohol. Consuming alcohol before the age of 18 also increases the risk of numerous poor developmental and social outcomes.

Settings and their associated customs and norms can influence how much alcohol we consume. People will often consume more alcohol in settings like bars, nightclubs and sports clubs, for example. This is usually because alcohol in these settings is sold, managed and marketed in ways that encourage easier or greater consumption.

People should be aware of this phenomoneon and try to consciously consume moderate amounts in these types of settings.

Symptoms of drinking too much

While all drinking has elements of long- and short-term risk, consistent drinking can lead to dependence and other alcohol-related problems. If you find it hard to stop drinking after you have started, you do things that are not normally expected of you because of your drinking, or you feel you sometimes need a drink in the morning, you may be showing signs of dependence and should consult your GP or a health practitioner.

Another sign of dependence is that, over time, greater amounts of alcohol are required to achieve intoxication. Persistent use and being preoccupied with your consumption, despite evidence of harm, is another sign your drinking might be unhealthily habitual.

If you feel guilty after drinking, have injured someone because of your drinking, or someone has suggested you reduce your drinking, you should also consider talking to someone about your alcohol consumption.

Steps to reduce alcohol consumption

While alcohol is part of our world, we can reduce the risk of short-term harm, disease and dependence. For adults, it is advised you have no more than two standard drinks a day. On any one day it is advised adults should not consume more than four standard drinks in a session.

A good way to cut down on your drinking is to start by ensuring you are having at least one to two alcohol-free days. On these days, you may want to substitute an alcoholic drink with something else, like sugar-free tonic water. This has a sophisticated taste but has no calories or alcohol.

Because of the long- and short-term risks, there should always be room to reduce your alcohol consumption. Perhaps in the long term you could try to avoid consumption during weekdays.

When going to functions where alcohol will be available, have a strategy rehearsed in your mind as to how and why you will not consume alcohol. You may say it is one of your alcohol-free days, you are not drinking today, or you are pacing yourself this week.

People are more health-conscious these days so tend to be more open about not drinking for health and well-being reasons. A non-alcoholic substitute drink will help you feel more socially integrated in these settings.

We should also ensure our children avoid alcohol before the age of 18. This is the safest way of maximising their health and human potential.

Food comas’, or why eating sometimes makes you sleepy

Health Check: ‘food comas’, or why eating sometimes makes you sleepy

September 21, 2015 2.32pm AEST

Here’s a clue: what you eat is just as important as the size of your meal. Dave Chiu/Flickr, CC BY-NC-ND

We’ve all done it, enjoyed a delicious meal only to nod off in a comfy chair for a while. For some of us, this is just a habit. But for others, it’s unavoidable. So what is it about food that can make us so sleepy?

When we’re eating, the stomach is producing gastrin, a hormone that promotes the secretion of digestive juices. As the food enters the small intestine, the cells in the gut secrete even more hormones (enterogastrone) that signal other bodily functions, including blood flow regulation.

But what does this have to do with sleepiness? Well, as we’re digesting our meal, more of our blood is shunted to the stomach and gut, to transport away the absorbed newly digested metabolites. This leaves less blood for the rest of the body and can cause some people to feel a bit “light-headed” or tired.

Still, the body is a lot more sophisticated than that; it doesn’t respond to food volume alone. What you eat is just as important as the size of your meal.

Biochemistry and sleep

For many years now, researchers have been investigating the link between food and sleepiness, but from another perspective. If we understand more about people’s sleep patterns, we might gain insight into what causes some people to put on weight and develop diseases such diabetes and atherosclerosis (a disease of the arteries that develops with fat deposits in artery walls).

We’ve known for many years that meals with an imbalance of nutrients – that are rich in either fats or carbohydrates – are associated with feeling sleepy. But this is not the case when nutrients are balanced or the meal is rich in protein. And that leads to the burning question: what is causing this effect?

Scientists in Germany have documented that meals high in carbohydrates that also have a high glycaemic index (meaning they release sugar into the bloodstream quickly) cause an increase in the hormone insulin. Insulin promotes the absorption and use of glucose from the bloodstream after a meal. But it also allows the entry of a special amino acid (we get these from the digestion of proteins), called tryptophan, into the brain.

This is important as tryptophan is converted into another chemical in the brain called serotonin, a signalling chemical or neurotransmitter that can be associated with calmness and drowsiness, especially in children.

But does eating foods rich in the essential amino acid tryptophan, such as turkey meat, cottage cheese, tofu and bananas, automatically make you sleepy? Probably not, as it’s the insulin surge brought about by ingesting carbohydrates that will allow the tryptophan to enter your brain, along with some other amino acids.

An imbalance of nutrients – meals that are rich in either fats or carbohydrates – are associated with feeling sleepy. Robbert Michel/Flickr, CC BY-NC-ND

Consuming a high-protein meal, on the other hand, will cause a lot of amino acids to enter the brain and will probably have a stimulant effect rather than a soporific one as the insulin released after eating stimulates their transport across cell membranes.

Cow’s milk drunk warm, often in the evening, for instance, is associated with sleepiness. But it’s the melatonin (a natural hormone that regulates our night or day rhythm) in the milk that can make us sleepy.

First identified in the 1950s, melatonin is a hormone secreted by the pineal gland under the brain. It’s mostly secreted at night, peaking around three or four in the morning. Melatonin acts on receptors in a part of the brain called the suprachiasmic nucleus (a cluster of cells) that triggers sleepiness as part of our sleep-wake cycle. Interestingly, melatonin is found in greater amounts in the milk of cows milked in night-time darkness, as opposed to in the daytime.

Sleep recipes

So overall, where are we now with our understanding of how food influences sleep? The short answer is that it’s complicated and we don’t yet fully understand it.

We know the gut hormones called enterogastrones, which are released when we eat, can influence blood flow. And that some of these hormones (especially one called CCK or cholecystokinin) can directly make us sleepy, probably by influencing the production of the neurotransmitter serotonin and melatonin.

We also know carbohydrates can promote the release of insulin after a meal, which may promote the actions of tryptophan on the brain, again via serotonin.

But to more practical matters: what should you do to avoid nodding off after a meal?

Here are a few suggestions:

  1. Don’t overeat; watch your portion size. Allow time during your meal for the level of your body’s natural hormones leptin (which reduces hunger) to rise and ghrelin (normally only released when we initiate eating) to fall, thereby lowering your appetite and inducing a feeling of satiety.
  2. Balance your meal; have protein and carbohydrate in roughly a one-to-two proportion. Include plant-based or marine-based fats rather than animal-based saturated fats in your meal. And don’t neglect any of the major food groups (vegetables and legumes, fruit, grains, lean meats and dairy products), as they all contain some essential nutrients that our bodies cannot manufacture.
  3. In particular, ensure you are getting all the minerals and micronutrients you need by including a variety of vegetables or salads in your diet, and a modest amount of fruit.
  4. Avoid “veging out” after the main meal of the day. Once the meal has settled, be moderately active. This will help promote better blood sugar control.

Good eating.

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

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


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

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



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.


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.


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).


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

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


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