Hormones: They control the human circadian rhythm, cause happiness after physical exercise, cause butterflies in one’s stomach and contribute to the chemistry of love, turn a pregnant woman’s life upside down and influence the growth of the fetus, in short, they are essential in the human individual development and homeostasis of organs. Hormones are mainly produced in the brain, pancreas, thyroid, kidney and the genital organs and represent the most important chemical messengers in the human organism. Hormone-dependent pathologic conditions are manifold and dysregulations need to be treated in order to warrant a healthy human body. Idiopathic short stature of children can e. g. be treated with growth hormones and researchers analyze the impact of hormone replacement therapy on well-being and health in the elderly [1, 2]. Hormones even enable the treatment of gender dysphoria, relieving the immense mental burden of the affected individuals . In order to understand the complex functions of hormones, nowadays a lot of research is being conducted. This review will give a short overview of the latest reports published in Acta Physiologica about the research on the regulation of hormones and recently identified ways of how hormones modulate the human metabolism. This article is protected by copyright. All rights reserved.
I have discussed this topic on many occasions, and have much more information on my website under Breast screening- mammography. All women should be informed about this important topic. Be aware of the many vested interests who cloud this debate.
Climacteric. 2018 Jan 17:1-5. doi: 10.1080/13697137.2017.1392503. [Epub ahead of print]
The role of screening mammography in the era of modern breast cancer treatment.
The evidence is reviewed on the efficacy and effectiveness of mammography screening derived from randomized screening trials and from the surveillance of populations where mammography screening for breast cancer has been introduced. Nearly all the trials were performed in the era before modern adjuvant therapy for breast cancer was introduced, apart from the Canadian National Breast Screening Study and the UK Age trial. The former found no benefit from annual mammography screening for 5 years in women age 40-59 years, the latter, a non-significant benefit from screening women by annual mammography for 7 years from ages 39 to 41 years. The evidence from population-based surveillance is mixed, most such studies having failed to consider the benefit gained from improved therapy.
It is concluded that we have reached the point of negligible benefit from mammography screening for breast cancer in women at average risk, and that we should concentrate on early diagnosis of breast cancer and the application of modern therapy according to clearly defined sub-types of breast cancer.
Professor, School of Biotechnology and Biomolecular Sciences, UNSW
Andrew Brown 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 their academic appointment.
On a species level, genes are implicated. But for individuals, genes don’t have as much of an effect as we may think. Let me explain.
Compared to our primate cousins, we humans are the “fat ape”. We store away more energy supplies in the form of body fat than gorillas, chimpanzees or orangutans. So the idea is that we have evolved to tuck away more fat energy to power our bigger brains.
However, for an individual, genes may not play such a huge role. About 100 genes so far have been linked to body weight, but together these explain less than 3% of variation in body mass index (BMI).
The biggest contributing gene, identified from genome-wide association studies, was the very logically named fat mass and obesity-associated gene (FTO). The BMI-increasing FTO variant is relatively common, present in up to 42% of the population and may add an extra kilogram or so to body weight.
However, this FTO gene only explains 0.3% variation in BMI. The even better news is people with this variant can lose weight just as easily through eating less and moving more.
So it’s good to remember genes don’t operate in isolation, but in cahoots with the food we eat and the physical activity we do.
It’s a rather odd thought that we share our bodies with 30 trillion or so bacteria. That’s about one bug for each one of our human cells. Many of these bugs live in our guts and their effect on various ailments, including obesity, is being studied intensively.
Probiotic supplements contain living bacteria, such as Lactobacillus, and prebiotics are a type of fibre that may improve gut health by favouring the growth of more gut-friendly strains of bacteria.
A summary of 13 studies found taking probiotic supplements for up to three months reduced body weight by 0.6 kg on average. Another recent summary of 18 studies combining data from treatments with prebiotics and/or probiotics came to a similar conclusion. That is, there was only an average 0.6 kg decrease in body weight.
Another, perhaps less palatable way to improve the profile of our gut bugs is by poo transplantation. However, we must await large systematic studies of poo transplants on weight loss before we can say if they help or not.
We often hear about energy intake referred to as calories, but the metric unit of measure is the joule, with one Calorie equalling 4.2 kilojoules.
In theory, if you decrease the kilojoules you consume by 10%, you should lose 10% body weight.
This theory was put to the test and found to be accurate by a study on 117 healthy participants over two years.
Conversely, elevated energy intake predicted weight gain in 253 participants followed over two years. The energy intake had to be carefully and objectively measured, as self-reporting underestimated energy intake by 35%.
If a kilojoule is a kilojoule, you should also be able to lose weight just the same if the kilojoule comes from fat or from carbohydrate, as long as there are fewer kilojoules overall. And that’s pretty much what was found in a summary of 32 controlled feeding studies, which compared different ratios of fat to carbohydrate but had the same reduced energy intake.
So our genes and gut bugs can influence weight gain, but the effects are relatively modest. Kilojoules, on the other hand, hold the master key to body weight regulation. Weight gain occurs when more kilojoules are consumed as food, rather than used for fuel.
Joseph Paul Forgas receives funding from the Australian Research Council.
Homo sapiens is a very moody species. Even though sadness and bad moods have always been part of the human experience, we now live in an age that ignores or devalues these feelings.
In our culture, normal human emotions like temporary sadness are often treated as disorders. Manipulative advertising, marketing and self-help industries claim happiness should be ours for the asking. Yet bad moods remain an essential part of the normal range of moods we regularly experience.
It’s time to re-assess the role of bad moods in our lives. We should recognise they are a normal, and even a useful and adaptive part of being human, helping us cope with many everyday situations and challenges.
A short history of sadness
In earlier historical times, short spells of feeling sad or moody (known as mild dysphoria) have always been accepted as a normal part of everyday life. In fact, many of the greatest achievements of the human spirit deal with evoking, rehearsing and even cultivating negative feelings.
Greek tragedies exposed and trained audiences to accept and deal with inevitable misfortune as a normal part of human life. Shakespeare’s tragedies are classics because they echo this theme. And the works of many great artists such as Beethoven and Chopin in music, or Chekhov and Ibsen in literature explore the landscape of sadness, a theme long recognised as instructive and valuable.
Ancient philosophers have also believed accepting bad moods is essential to living a full life. Even hedonist philosophers like Epicurus recognised living well involves exercising wise judgement, restraint, self-control and accepting inevitable adversity.
Other philosophers like the stoics also highlighted the importance of learning to anticipate and accept misfortunes, such as loss, sorrow or injustice.
What is the point of sadness?
Psychologists who study how our feelings and behaviours have evolved over time maintain all our affective states (such as moods and emotions) have a useful role: they alert us to states of the world we need to respond to.
In fact, the range of human emotions includes many more negative than positive feelings. Negative emotions such as fear, anger, shame or disgust are helpful because they help us recognise, avoid and overcome threatening or dangerous situations.
But what is the point of sadness, perhaps the most common negative emotion, and one most practising psychologists deal with?
Intense and enduring sadness, such as depression, is obviously a serious and debilitating disorder. However, mild, temporary bad moods may serve an important and useful adaptive purpose, by helping us to cope with everyday challenges and difficult situations. They also act as a social signal that communicates disengagement, withdrawal from competition and provides a protective cover. When we appear sad or in a bad mood, people often are concerned and are inclined to help.
Some negative moods, such as melancholia and nostalgia (a longing for the past) may even be pleasant and seem to provide useful information to guide future plans and motivation.
Sadness can also enhance empathy, compassion, connectedness and moral and aesthetic sensibility. And sadness has long been a trigger for artistic creativity.
Recent scientific experiments document the benefits of mild bad moods, which often work as automatic, unconscious alarm signals, promoting a more attentive and detailed thinking style. In other words, bad moods help us to be more attentive and focused in difficult situations.
In contrast, positive mood (like feeling happy) typically serves as a signal indicating familiar and safe situations and results in a less detailed and attentive processing style.
Psychological benefits of sadness
There is now growing evidence that negative moods, like sadness, has psychological benefits.
To demonstrate this, researchers first manipulate people’s mood (by showing happy or sad films, for example), then measure changes in performance in various cognitive and behavioural tasks.
Feeling sad or in a bad mood produces a number of benefits:
better memory In one study, a bad mood (caused by bad weather) resulted in people better remembering the details of a shop they just left. Bad mood can also improve eyewitness memories by reducing the effects of various distractions, like irrelevant, false or misleading information.
more accurate judgements A mild bad mood also reduces some biases and distortions in how people form impressions. For instance, slightly sad judges formed more accurate and reliable impressions about others because they processed details more effectively. We found that bad moods also reduced gullibility and increased scepticism when evaluating urban myths and rumours, and even improved people’s ability to more accurately detect deception. People in a mild bad mood are also less likely to rely on simplistic stereotypes.
motivation Other experiments found that when happy and sad participants were asked to perform a difficult mental task, those in a bad mood tried harder and persevered more. They spent more time on the task, attempted more questions and produced more correct answers.
better communication The more attentive and detailed thinking style promoted by a bad mood can also improve communication. We found people in a sad mood used more effective persuasive arguments to convince others, were better at understanding ambiguous sentences and better communicated when talking.
increased fairness Other experiments found that a mild bad mood caused people to pay greater attention to social expectations and norms, and they treated others less selfishly and more fairly.
Counteracting the cult of happiness
By extolling happiness and denying the virtues of sadness, we set an unachievable goal for ourselves. We may also be causing more disappointment, some say even depression.
University of Helsinki and Helsinki University Hospital, Department of Obstetrics and Gynecology, Helsinki, Finland.
Folkhälsan Research Center, Biomedicum, Helsinki, Finland.
EPID Research Oy, Espoo, Finland.
National Institute for Health and Welfare, Helsinki, Finland.
Karolinska Institute, Department of Neurobiology, Care Sciences and Society, Division of Family Medicine, Stockholm, Sweden.
The aim of the study was to evaluate the risk of cardiac and stroke deaths in women who discontinue postmenopausal hormone therapy (HT).
We analyzed the risk of death due to cardiac (n = 5,204) and cerebrovascular (n = 3,434) causes in Finnish women who discontinued systemic HT during 1994 to 2013 (n = 432,775). The risks were compared with those in the age-matched female background population and with those in age-matched HT users. Women diagnosed with cardiac or cerebrovascular events within 1 year before discontinuation of HT were excluded (n = 8,711).
Women younger than 60 years at discontinuation of HT showed a significantly increased risk of cardiac death (after ≤5 y of HT exposure, standardized mortality ratio [SMR] 1.52, 95% CI 1.13-2.00; after >5 y of exposure, SMR 2.08, 95% CI 1.44-2.90) and stroke death (after ≤5 y of exposure, SMR 2.62, 95% CI 2.07-3.28; after >5 y of exposure, SMR 3.22, 95% CI 2.29-4.40) during the first year after treatment as compared with age-matched female background population. When compared with HT users, elevations in risks of cardiac and stroke deaths were even higher. Increased mortality risks were limited to the first post-HT year because increases in risks vanished or markedly decreased when the follow-up time was extended over more than 1 year.
Discontinuation of postmenopausal HT may be associated with increased risk of cardiac and stroke death in the first posttreatment year. Further investigation is required to evaluate causality of the observed associations.
Risk factors are characteristics that increase the likelihood of developing a disease, such as a cancer. There are different types of risk factors; some can be modified (diet, physical activity) while others can’t (age, genetic factors). Sometimes, risk factors can be modified by some people but not others (e.g., the number of children).
Although certain factors can increase a woman’s risk for developing gynaecological cancer, they do not always cause the cancer. Many women carry at least one risk factor but still will not develop gynaecological cancer. Even if a woman with a gynaecological cancer carries a risk factor, it is difficult to know how much that risk factor contributed to the development of cancer.
Risk factors also look to explain cancer incidence of larger populations but sometimes it will be impossible to attribute “fault” to a risk factor. For example, cervical cancer is caused by Human Papilloma Virus (HPV), which is a sexually transmitted virus. However, the vast majority of women will have sexual intercourse at least once in their lives without developing cervical cancer. It remains unknown why some women develop cancer and others don’t.
While the causes of some gynaecological cancers are not fully understood some known risk factors include:
Increasing age. The risk of a woman being diagnosed with gynaecological cancer increases beyond the age of 65 years.
Reproductive history such as child-bearing. Women who have never given birth, who had infertility issues, never breastfed or had their first child after the age of 30 are at increased risk for ovarian cancer.
Exposure to hormones produced by the body or taken as medication. For e.g, estrogen-only hormone replacement therapy (HRT) taken as tablets after menopause may be associated with an increased risk of uterine cancer.
Previously diagnosed with cancer. A woman who has had any previous cancer diagnosis may have an increased risk of developing any type of cancer in the future. For example, women who developed breast cancer are at a significantly higher risk of developing uterine and ovarian cancer.
Exposure to diethylstilbestrol (DES) in the womb. DES is a synthetic form of the hormone estrogen. Doctors prescribed DES to help some pregnant women to prevent miscarriage between the 1940s and 1970s in Australia. Women whose mothers were given DES during pregnancy may be at increased risk of cervical and vaginal cancer.
Viral infection such as Human Papilloma Virus (HPV). Certain types of HPV have been linked to the development of cervical cancer.
The oral contraceptive pill. Long-term use of the oral contraceptive pill is associated with a small increased risk of cervical cancer. However, the pill has a substantial (50%) and long-lasting protective effect against ovarian and endometrial cancer.
Being overweight. Increased caloric intake and obesity is strongly linked to an increased risk of endometrial cancer. Regarding ovarian cancer and cervical cancer, the evidence is less consistent.
Diet. A diet low in fruit, vegetables and grains, and high in saturated fat may increase ovarian cancer risk.
It is important for women to know their risk factors and talk about them with health professionals if concerned. Knowing cancer risk factors can prompt an individual to make lifestyle choices that may decrease cancer risk and improve overall health. Knowing risk factors could also aid in deciding if genetic testing may be an option.
Estradiol (E2) is women’s dominant ‘bone hormone’ since it is essential for development of adolescent peak bone mineral density (BMD) and physiological levels prevent the rapid (3-week) bone resorption that causes most adult BMD loss. However, deceasing E2 levels trigger bone resorption/loss. Progesterone (P4) is E2’s physiological partner, collaborating with E2 in every cell/tissue; its bone ‘job’ is to increase P4-receptor-mediated, slow (3-4 months) osteoblastic new bone formation. When menstrual cycles are normal length and normally ovulatory, E2 and P4 are balanced and BMD is stable. However, clinically normal cycles commonly have ovulatory disturbances (anovulation, short luteal phases) and low P4 levels; these are more frequent in teen and perimenopausal women and increased by everyday stressors: energy insufficiency, emotional/social/economic threats and illness. Meta-analysis shows that almost 1%/year spinal BMD loss occurs in those with greater than median (∼31%) of ovulatory disturbed cycles. Prevention of osteoporosis and fragility fractures requires the reversal of stressors, detection and treatment of teen-to-perimenopausal recurrent cycle/ovulatory disturbances with cyclic oral micronized progesterone. Low ‘Peak Perimenopausal BMD’ is likely the primary risk for fragility fractures in later life.
Progesterone plus estradiol or other antiresorptive therapies adds 0.68%/year and may be a highly effective osteoporosis treatment. Randomized controlled trials are still needed to confirm progesterone’s important role in women’s bone formation.
Lecturer In Nutritional Sciences, Deakin University
Gunveen Kaur 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.
Turmeric is a yellow coloured spice widely used in Indian and South East Asian cuisine. It’s prepared from the root of a plant called Curcuma longa and is also used as a natural pigment in the food industry.
In the literature, curcumin is reported to be an antioxidant that protects the body against damage from reactive molecules. These are generated in the body as a result of metabolism and cause cell damage (known as free radicals).
It’s also reported to have anti-inflammatory, anti-bacterial and anti-cancer properties, as well as encouraging the death of cells that are dangerous or no longer needed by the body.
Curcumin has been widely studied in relation to numerous ailments, but what does the literature say? Is consuming turmeric beneficial?
For aches and pains
Chronic inflammation has been linked to the development of numerous diseases such as obesity, diabetes,heart disease and cancer. There is some evidence curcumin reduces the levels of certain substances (cytokines) that produce inflammation.
Systematic reviews and meta-analyses, which combine data from several randomised controlled trials (where an intervention is tested against a placebo, while the subjects and those conducting the study don’t know who has received which treatment) support this finding to a certain extent.
A meta-analysis of nine randomised controlled trials showed taking curcumin supplements led to a significant reduction in cytokines that produce inflammation. But the authors claimed these reductions were modest, and it’s unclear if they would actually have a benefit in real life.
These trials were conducted with small sample sizes ranging from 10 to 50 people, which reduces the strength of the evidence. It’s difficult to draw a conclusion on a beneficial dose and how long you should take curcumin, or the population group that can benefit the most from curcumin.
A meta-analysis investigated the effects of turmeric/curcumin on pain levels in joint arthritis patients. The group supplemented with 1000mg of curcumin per day said they had reduced pain compared with the placebo group.
In this study, curcumin was found to be as effective as ibuprofen in terms of reducing pain levels in these patients. But the authors of this meta-analysis themselves suggested that due to small sample size and other methodological issues there is not sufficient evidence to draw definitive conclusions.
For diabetes and heart disease
Curcumin is also thought to be beneficial in preventing insulin resistance (which leads to increased blood sugar), improving high blood sugar and reducing the toxic effects of high blood glucose levels.
But these studies have been conducted in animals and are very few humantrials have been conducted in this area.
One study that reported reduction in blood glucose levels in type 2 diabetes patients reports a change in blood glucose from 8.58 to 7.28 millimoles per litre after curcumin supplementation. People with levels above seven are classified as diabetics. So in clinical terms, the change is not that much.
Similarly in relation to heart disease, animal studies show benefits of curcumin supplementation in improving heart health, but there are very few clinical trials conducted in heart disease patients.
Smaller clinical trials looking at ten patients also show benefits of curcumin in reducing serum cholesterol, which is a risk factor for heart disease. But meta-analysis looking at combined effects of different trials does not show these benefits.
There is some evidence curcumin lessens the severity of side-effects from radiation therapy such as radiation-induced dermatitis and pneumonitis (inflammation of lungs), but not the cancer itself.
Research shows not all curcumin we take orally is absorbed. This has led to the use of other things such as lipids (fats) and piperine (found in black pepper), to help it absorb into our system.
High intakes (up to 12 grams a day) of curcumin can cause diarrhoea, skin rash, headaches and yellow-coloured faeces. Looking at the Indian population, they consume about 100mg of curcumin a day, which corresponds to 2 to 2.5 grams of turmeric per day.
But they also consume these amounts over relatively long periods of time (typically their lifespan). There are reports of lower cancer rates in the Indian population and this has been linked to turmeric consumption, but there are no longer term trials proving this link.
It appears that in order to receive benefits from high doses over a short period of time, people are now resorting to injecting turmeric intravenously. There is no evidence to support the benefits of high doses of turmeric or IV injections of turmeric at all.
Although curcumin is showing some encouraging effects in reducing markers of inflammation in humans, the majority of the pharmacological effects of curcumin are in lab studies or animal experiments. Until there are more high quality randomised controlled trials conducted to confirm the benefits of curcumin or turmeric, it’s best to consume turmeric orally as a spice as part of a healthy, nutritious diet.
Division of Preventive Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts.
Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington.
National Heart, Lung, and Blood Institute, Bethesda, Maryland.
Department of Family Medicine and Public Health, University of California, San Diego, School of Medicine, San Diego.
Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance.
now with City of Hope National Medical Center, Department of Medical Oncology and Therapeutics Research, Duarte, California.
MedStar Health Research Institute, Washington DC.
Georgetown/Howard Universities Center for Clinical and Translational Sciences, Washington DC.
Department of Health Promotion Sciences, Mel and Enid Zuckerman College of Public Health, University of Arizona, Tucson.
HealthPartners Institute for Education and Research, Minneapolis, Minnesota.
Division of Preventive Medicine, University of Alabama at Birmingham, Birmingham.
Stanford Prevention Research Center, Stanford University School of Medicine, Stanford, California.
Department of Medicine, The Ohio State University, Columbus.
Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis.
Cardiology Division, George Washington University School of Medicine and Health Sciences, Washington DC.
Department of Social Sciences and Health Policy, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Department of Biostatistical Sciences, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Department of Epidemiology and Environmental Health, University at Buffalo, Buffalo, New York.
Health outcomes from the Women’s Health Initiative Estrogen Plus Progestin and Estrogen-Alone Trials have been reported, but previous publications have generally not focused on all-cause and cause-specific mortality.
To examine total and cause-specific cumulative mortality, including during the intervention and extended postintervention follow-up, of the 2 Women’s Health Initiative hormone therapy trials.
Design, Setting, and Participants:
Observational follow-up of US multiethnic postmenopausal women aged 50 to 79 years enrolled in 2 randomized clinical trials between 1993 and 1998 and followed up through December 31, 2014.
Conjugated equine estrogens (CEE, 0.625 mg/d) plus medroxyprogesterone acetate (MPA, 2.5 mg/d) (n = 8506) vs placebo (n = 8102) for 5.6 years (median) or CEE alone (n = 5310) vs placebo (n = 5429) for 7.2 years (median).
Main Outcomes and Measures:
All-cause mortality (primary outcome) and cause-specific mortality (cardiovascular disease mortality, cancer mortality, and other major causes of mortality) in the 2 trials pooled and in each trial individually, with prespecified analyses by 10-year age group based on age at time of randomization.
Among 27 347 women who were randomized (baseline mean [SD] age, 63.4 [7.2] years; 80.6% white), mortality follow-up was available for more than 98%. During the cumulative 18-year follow-up, 7489 deaths occurred (1088 deaths during the intervention phase and 6401 deaths during postintervention follow-up). All-cause mortality was 27.1% in the hormone therapy group vs 27.6% in the placebo group (hazard ratio [HR], 0.99 [95% CI, 0.94-1.03]) in the overall pooled cohort; with CEE plus MPA, the HR was 1.02 (95% CI, 0.96-1.08); and with CEE alone, the HR was 0.94 (95% CI, 0.88-1.01). In the pooled cohort for cardiovascular mortality, the HR was 1.00 (95% CI, 0.92-1.08 [8.9 % with hormone therapy vs 9.0% with placebo]); for total cancer mortality, the HR was 1.03 (95% CI, 0.95-1.12 [8.2 % with hormone therapy vs 8.0% with placebo]); and for other causes, the HR was 0.95 (95% CI, 0.88-1.02 [10.0% with hormone therapy vs 10.7% with placebo]), and results did not differ significantly between trials. When examined by 10-year age groups comparing younger women (aged 50-59 years) to older women (aged 70-79 years) in the pooled cohort, the ratio of nominal HRs for all-cause mortality was 0.61 (95% CI, 0.43-0.87) during the intervention phase and the ratio was 0.87 (95% CI, 0.76-1.00) during cumulative 18-year follow-up, without significant heterogeneity between trials.
Conclusions and Relevance:
Among postmenopausal women, hormone therapy with CEE plus MPA for a median of 5.6 years or with CEE alone for a median of 7.2 years was not associated with risk of all-cause, cardiovascular, or cancer mortality during a cumulative follow-up of 18 years.
Emily Burch 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 their academic appointment.
Researchers started exploring the link between diet and skin health, particularly acne, in the mid-1900s. Dermatology textbooks from the 1930s advised restricting carbohydrates, sweets and junk foods to improve acne. But these recommendations were based on doctors’ experiences and observations, not quality research.
Chocolate is one junk food that often gets blamed as an aggravating factor of acne. In a 1969 study, 65 people with acne were asked to eat one chocolate bar per day for four weeks. They were either given a bar that contained ten times the amount of chocolate found in a typical bar, or a bar that looked identical but contained no chocolate.
Results showed participants who ate the chocolate bars did not have more breakouts than those who didn’t eat the chocolate.
Similar results were found in a 1971 study. Twenty-seven students who reported being sensitive to dietary acne triggers ate large amounts of chocolate, milk, roasted peanuts or soft drinks for one week. No significant difference in the number of breakouts was observed between the groups.
But these studies also had some major limitations. The 1969 study was sponsored by the Chocolate Manufacturers Association of the United States of America. And both studies did not assess participants’ intake of other foods during the study period, which may have influenced their complexion.
More recently, a 2011 study including ten men aged between 18-35 found significant changes occurred in the severity of acne after a single intake of pure chocolate (100% cocoa). There was a strong association between the amount of chocolate consumed and the number of breakouts four and seven days after they ate the chocolate.
So overall, study findings show conflicting results, and clear recommendations about chocolate cannot yet be made.
But better-quality research does suggest other dietary strategies worth trying if you want to improve your skin. These include eating more fruits and vegetables as well as foods with a lower glycaemic load.
The glycaemic index (GI) is a ranking between 0-100 given to carbohydrate-containing foods to describe how quickly the carbohydrates are digested into glucose (sugar) and absorbed into our blood. The lower the GI, the slower the rise in blood glucose levels when the food is consumed. Most junk foods (candy, chips and cakes) have a high GI.
Glycaemic load (GL) builds on the concept of GI but also considers the amount of food being eaten. This provides a more accurate picture of the overall effect the food has on blood glucose levels.
Once the glucose enters the blood, a hormone called insulin moves it into our cells to be used for energy. Diets with a high GL trigger a higher response in insulin. This high level of insulin increases a hormone called the insulin-like growth factor (IGF), which has been associated with skin breakouts – like pimples.
In a 2008 randomised control trial (considered the gold standard in scientific research as it compares findings between two groups), 31 males with acne, aged 15-25, were asked to follow either a low-GL or a high-GL diet for 12 weeks. The low-GL group was instructed to substitute high-GI foods (processed cereals, potatoes and white bread and rice) with lower-GI foods (lean meats, fruits and wholegrain bread and pasta).
The high-GL group was encouraged to include carbohydrates as a regular part of their diet and wasn’t educated about GI. Those following the low-GL diet saw their acne improve and lost more weight.
A 2007 randomised controlled trial had similar findings. But because participants in both studies who were following the low-GL diet lost weight, it’s also possible improvements in their skin were due to weight loss and not the diet itself.
Fruit and vegetables
Fruits and vegetables are wonderful for our bodies in many ways, but research shows they can also give our skin a natural, healthy glow – by tinting it yellow and red.
Our skin colour is influenced by three pigments – haemoglobin, carotenoids and melanin. Many fruits and vegetables contain carotenoids. These are responsible for the deep green colour of broccoli and spinach, the vibrant orange colour of carrots and oranges, and the red hue of capsicums and tomatoes.
When you eat fruits and vegetables, these pigments can accumulate in your skin, leading to a healthy golden glow. The same benefits haven’t been seen with supplements, so it’s best to get your carotenoid hit from eating lots of different fruits and vegetables.
Milk naturally contains anabolic steroids, growth hormones and other growth factors. In a complicated metabolic pathway, these factors lead to a higher release of insulin and insulin-like growth factor, which can stimulate the development and progression of acne.
A number of studies have examined the alleged connection between milk and acne. In 2005, 50,000 women recalled their high school diet and were asked if they had ever been diagnosed with severe acne by their doctor.
Researchers found those who had a higher reported intake of milk (particularly skim milk) more commonly suffered from acne. A 2006 study with around 6,000 teenage girls and a 2008 study with around 4,700 teenage boys showed similar results.
But no randomised controlled trials have been conducted that examine the association between milk and acne. This means whether dairy is a cause of acne hasn’t yet been established. High-quality research is needed before specific recommendations can be made.
If you are trying to improve your skin’s complexion, you could try these strategies:
reduce high-GL foods by decreasing the amount of processed, junk food you eat
add low-GL foods that won’t spike your blood glucose levels (vegetables, sweet potatoes, barley, beans and multigrain bread)
eat a diverse range of fruits and vegetables to get a healthy glow.