Women who consume even modest amounts of fructose from sugar-sweetened beverages (eg, roughly two-thirds of a can of pop per day) are more likely to have elevated androgen levels, which may have implications for conditions such as acne and hirsutism.
METHODOLOGY:
Investigators performed a population-based cohort study among men and women aged 40-70 years from the UK Biobank.
In 136,384 individuals, they assessed associations of intake of various sources of fructose with levels of sex hormone–binding globulin (SHBG) and testosterone, and with hyperandrogenism (free androgen index > 4.5).
In 383,392 individuals, they assessed associations of a genetic variant that impairs fructose metabolism with hormone levels and acne.
TAKEAWAY:
Men and women consuming more total fructose and more fructose from fruit had higher SHBG levels and lower free testosterone levels; women had a lower risk for hyperandrogenism.
In contrast, men and women consuming at least 10 g/d of fructose from sugar-sweetened beverages — corresponding to 200 mL (about two-thirds of a can of pop) — had lower SHBG levels; women had higher free testosterone levels and were more likely to have hyperandrogenism (adjusted odds ratio [OR], 1.018).
Men and women who carried the genetic variant that impairs fructose metabolism had higher SHBG levels and a lower risk for acne (OR, 0.975).
Women carrying the variant had lower free testosterone levels and a lower risk for hyperandrogenism (adjusted OR, 0.997).
IN PRACTICE:
“The relevance of these findings is indicated by the high consumption of SSB [sugar-sweetened beverages] in certain age and socioeconomic groups and the high prevalence of disorders associated with hyperandrogenism, such as polycystic ovary syndrome and acne vulgaris,” the authors wrote. Eliminating the 10 g/d of fructose is “an easily implementable dietary change,” they added.
Researchers found that irisin, an exercise-induced hormone, improves cognitive performance in mice.
The hormone, which is identical in people, could potentially be used to treat cognitive disorders such as Alzheimer’s disease.
A study in mice may explain why exercise improves cognitive function during aging.
Exercise may benefit brain health and improve cognitive performance during aging. It’s also associated with reduced Alzheimer’s disease risk and cognitive decline. But the mechanisms responsible aren’t well understood. Factors secreted into the bloodstream may play a role. If so, these factors would be promising leads for developing treatments for cognitive disorders.
Past studies found that exercise induces production of FNDC5, a protein found on the surfaces of certain cells. FNDC5 can activate neuroprotective genes in the hippocampus, the brain region in charge of memory formation. The outer part of FNDC5 can be cleaved off to form a hormone called irisin, which is released into the bloodstream. A team of researchers, led by Dr. Christiane Wrann at Massachusetts General Hospital and Harvard Medical School, investigated whether irisin is responsible for mediating the cognitive benefits of exercise.
The study was supported in part by several NIH institutes (see below). Results appeared in Nature Metabolism on August 20, 2021.
First, the researchers deleted the gene encoding FNDC5 in mice, thereby removing irisin. They then compared the effects of exercise on cognitive performance in these “knockout” mice and in control mice. Some mice had an exercise wheel to run on, while others did not.
Control mice who could freely exercise showed improved cognitive performance over those that could not. But in the knockout mice, exercise made no difference in cognitive performance. The knockout mice also showed greater cognitive decline with age than control mice.
Next, the researchers delivered irisin directly into the mice’s brains. Doing so improved cognitive performance in both knockout and control mice.
The team examined the neurons in the knockout mice in a part of the hippocampus. They found that newly born neurons in this area had abnormal activation patterns, structure, and gene activity.
The researchers then tested the therapeutic potential of irisin in mouse models of Alzheimer’s disease. They delivered the gene for irisin into the mice, which led to irisin production in the liver. The blood of these mice, in turn, contained elevated irisin levels. Two months after treatment, the researchers tested the mice’s cognitive performance. The irisin-treated mice performed better on the tests than untreated mice. Treated mice also showed signs of reduced neuroinflammation—a process related to neurodegenerative diseases—in the hippocampus. In addition, the researchers found that irisin could cross the blood-brain barrier to act on the brain.
These results suggest that exercise may improve cognitive performance by increasing irisin levels. “This is particularly important inasmuch as irisin, a small natural peptide, would be much easier to develop into a therapeutic than the much larger membrane-bound protein FNDC5,” Wrann says.
Irisin is identical in mice and people. Its blood levels in people have also been shown to rise with endurance exercise. It could thus potentially help to treat a variety of cognitive disorders. Wrann adds, “since irisin does not specifically target amyloid plaques, but rather neuroinflammation directly, we’re optimistic it could have beneficial effects on neurodegenerative diseases beyond just Alzheimer’s.”
Rendering of SARS-CoV-2 spike proteins binding to ACE2 receptors.
Dr. Flavio Cadegiani, a Brazilian endocrinologist, suspects that the worst is yet to come for spike-protein-induced diseases in the endocrine system.
The endocrine system, colloquially known as the hormone system, is critical for our health. It regulates growth and development, mood, metabolism, reproduction, immunity, and functions of other organs through the secretion of hormones.
Hormones are one of the three biggest messengers in the body. Compared to the two other messengers—neurotransmitters and cytokines—hormones are slower in responding and have systemic functions across the body rather than localized actions.
While cells can usually respond to neurotransmitters in milliseconds and cytokines in minutes to hours, cells that respond to hormones can take hours or even weeks.
Since hormones can have slow and systemic actions, a dysfunctional or damaged endocrine system will generally be slow in its symptom onset and recovery.
Studieshave shown that spike proteins from COVID-19 infection and the COVID-19 vaccines can damage endocrine glands, including pituitary, thyroid, and adrenal glands, as well as reproductive organs and many more.
Cadegiani raised a concern that the slower onset of endocrine pathologies may pose difficulties in diagnosis and treatment.
Depletion of Hormonal Reserves
Endocrine pathologies can take longer to become apparent because endocrine glands have “reserves,” according to Cadegiani.
“What we’re going to see in the future [for endocrine diseases] is a little bit different from the other fields, because glands have reserves and the decrease of the reserve will not be clinically seen right now, but it may be in the future,” Cadegiani said at a Front Line COVID-19 Critical Care Alliance (FLCCC) conference in Kissimmee, Florida.
Therefore, affected individuals may show no symptoms until their reserves have been depleted.
Cadegiani said most of his concerns for the future are speculative and based on his own clinical observations. But since the pandemic and the administration of COVID-19 vaccines began, there have been increasing reports that implicate endocrine pathologies.
(udaix/Shutterstock)
Hormonal Axis and Systemic Dysfunction
Hormones regulate the entire body, so once the reserves are depleted and underlying endocrine pathologies are unmasked, there may be cases of systemic dysregulations.
Endocrine glands control the function of many organs across the body, and each endocrine organ is also connected through a feedback loop, also known as a hormonal axis.
At the top of this chain is the hypothalamus, which is a diamond structure in the brain and acts as a master switchboard. It sends messages to the pituitary gland, a small, oval structure tucked behind the nose.
The pituitary gland is colloquially known as the master gland; it regulates other endocrine organs together with the hypothalamus, forming hormonal axes.
The pituitary gland is part of the hypothalamic-pituitary-gonadal axis, which regulates the reproductive organs, including the ovaries and the testes. In females, it’s responsible for regulating the release of ovarian hormones as part of the menstrual cycle; in males the axis regulates spermatogenesis.
The hypothalamic-pituitary-adrenal axis is a neuroendocrine axis that mediates the adrenal glands, an organ that produces hormones that trigger the fight-or-flight response. The process is a stress response that occurs in response to harmful threats and can reduce metabolism, suppress the immune system, and activate the sympathetic nervous system.
Another major axis is the hypothalamic-pituitary-thyroid axis. This regulates the thyroid gland and the hormones it secretes. Thyroid hormones are essential for biological functions of growth, regulation of the cardiovascular system, bone replacement, liver function, and metabolism.
Spike proteins particularly favor tissues and organs that express ACE2 and CD147 receptors. Many endocrine glands display ACE2 receptors, including the pancreas, thyroid, testes, ovaries, adrenal gland, and pituitary gland, making the endocrine system particularly vulnerable to SARS-CoV-2.
The key driver behind spike-protein-induced disease is inflammation.
Upon entering cells, spike proteins can activate pro-inflammatory pathways by inducing DNA damage; inhibiting DNA repair; causing stress to the cell’s mitochondria, which is critical for cell energy production; and much more. All of this lead to cellular stress, injury, and possible cell death.
When many cells are affected, it can cause problems in tissues and organs, affecting individual endocrine glands and the system.
Spike proteins also inhibit autophagy, the cellular “recycling system,” thereby preventing the cells from clearing the toxic protein out, leading to prolonged damage.
Spike proteins may also contribute to autoimmunity. Since it shares many similarities with common human tissues and proteins—known as “molecular mimicry”—it has the potential to cause immune cells to mount an attack against the body’s own cells and organs, leading to endocrine damage.
Several studies have reported on endocrine pathologies following COVID-19, although data on the exact damage is still emerging.
(ttsz/iStock)
Pituitary Gland
As the master gland of the endocrine system, the pituitary gland secretes many hormones, including ones that regulate other endocrine glands:
Adrenocorticotrophic hormone (ACTH) targets the adrenal glands and is responsible for producing cortisol, which stimulates the stress response.
Thyroid-stimulating hormone regulates the thyroid.
Growth hormone is responsible for growth and metabolism.
Melanocyte-stimulating hormone boosts the production of melanin when exposed to UV rays and increases appetite.
Antidiuretic hormone is responsible for retaining water and producing less urine.
Luteinizing hormone (LH) follicle-stimulating hormone (FSH), and prolactin are important for reproduction.
Oxytocin plays a role in childbirth, metabolism, and happiness.
Studies in cell culture have shown that the spike proteins are able to suppress the production of LH and FSH in pituitary cells, with unknown long-term consequences in humans.
ACTH deficiencies have been observed following mRNA vaccination in Japan, with the person affected found to have a shrunken pituitary gland.
Cadegiani said pathologies in the pituitary are difficult to diagnose; they’re often masked by other conditions, therefore there’s little literature on pituitary pathology presentation after COVID-19 vaccinations.
The adrenals are a pair of glands shaped like Napoleon’s hat that sit just above the kidneys. (ttsz /iStock)
Adrenal Glands
There’s published literature with data that may be used as evidence to suggest spike protein injury at the adrenal glands.
The adrenal glands, located above the kidneys, produce hormones responsible for the stress response. This includes adrenaline, cortisol, and aldosterone. The release of these three hormones is critical for maintaining energy and other needs during stressful situations.
The glands are also likely to be involved in post-vaccine myocarditis events that are often seen in young males. Cadegiani said this type of myocarditis may be a sign of adrenal dysfunction.
Cadegiani authored a peer-reviewed study on post-vaccine myocarditis and concluded that catecholamines are a main trigger for these events. Catecholamines are a group of neurohormones and include dopamine, noradrenaline, and adrenaline.
While dopamine mostly acts within the nervous system, both adrenaline and noradrenaline play important roles in stress responses.
Adrenaline activates the fight-or-flight stress response and the noradrenaline supports the response by increasing heart rate, breaking down fats, and increasing blood sugar levels.
Intense and prolonged exercise triggers the fight-or-flight response, which is why catecholamines are usually elevated in athletes. Males, in particular, tend to have higher levels of catecholamine. Testosterone is also suspected to play a role in the higher incidence of myocarditis following vaccination.
Cadegiani linked catecholamines with myocarditis by analyzing the autopsy reports of two teenage boys who died three to four days after mRNA vaccination from myocarditis events. Their heart damage was different from normal myocarditis pathology, with clear similarities with stress-induced cardiomyopathy; Cadegiani observed clear characteristics of catecholamine-induced myocarditis.
He hypothesized that the vaccines triggered a hyper-catecholaminergic state by elevating levels of adrenaline, causing hyperactivation of adrenaline.
Studies on mRNA-vaccinated athletes also found that after exercise, those who were vaccinated had higher heart rates and noradrenaline levels than those who weren’t vaccinated.
Dysfunctions in the adrenal glands are likely to lead to adrenal insufficiency.
Cadegiani hypothesized adrenal insufficiency—a condition in which the adrenal glands become unable to produce enough hormones—to be a possible consequence of spike protein injury.
There’s already a report of adrenal insufficiency following infection; in the case of long COVID in which there are spike protein remnants, it’s likely that the damage will be prolonged, possibly leading to chronic damage.
In the case of vaccines, a report evaluating spike protein production after COVID-19 mRNA vaccination found that the adrenal gland was one of the highest spike protein-producing tissues, and the spike protein production in the gland increased with time.
Current research has also shown that complications from thrombocytopenia as a post-vaccine symptom have led to adrenal hemorrhage and adrenal insufficiency.
The thyroid is a butterfly-shaped gland located in the neck just above the collarbone. It secretes hormones that regulate many body functions, including metabolism and cell growth. (Shutterstock)
Thyroid
The thyroid is a butterfly-shaped gland located over the throat. It has a lot of functions, primarily regulating growth and metabolism.
It makes two hormones: thyroxine and triiodothyronine. Deficiencies in triiodothyronine results in hypothyroidism, characterized by a large thyroid; over-secretion of it can cause hyperthyroidism.
The thyroid also plays a role in regulating the immune system. COVID-19 infection is often a sign of underlying thyroid problems, and damage from infection can exacerbate thyroid problems, creating a negative cycle.
An autopsy study on 15 people deceased from COVID-19 found that 13 of them had viral RNA and proteins in their thyroid tissues. ACE2 receptors, previously thought to be not presented on the thyroid, were also detected, indicating a possible route for SARS-CoV-2 infection.
Although the research shows that thyroids can be implicated in infection, thyroiditis, which is inflammation of the thyroid, has currently only been reported in relation to the COVID-19 vaccine.
A study from Turkey states that the COVID-19 vaccine can induce thyroiditis. The study evaluated 15 patients who developed thyroiditis following vaccination.
Four of the patients also developed Graves’ disease, which is an autoimmune disease and a complication of hyperthyroidism. Hashimoto’s disease, another thyroid autoimmune condition, has also been reported following vaccinations.
It’s possible that spike proteins produced from vaccinations may attack the thyroid cells by binding to ACE2 receptors. However, looking at the high reports of autoimmune diseases, Cadegiani said the pathogenesis of thyroid dysfunction is likely autoimmune. The spike proteins have also demonstrated their autoimmune capacity due to high incidences of “molecular mimicry.”
Pancreas
The pancreas produces glucagon and insulin, two important hormones that regulate our blood sugar levels. Dysregulation of blood sugar levels is an indication of pancreatic dysfunction and may lead to complications, such as diabetes.
Spike proteins from both the vaccine and the virus have shown a potential to disturb glucose metabolism.
There have been reports of a sudden onset of type 1 diabetes, which is a form of autoimmune disease in which the body attacks its own pancreatic beta cells.
A study evaluating EudraVigilance safety surveillance reports also found reports of dysregulation of blood glucose with transient worsening of hyperglycemia reported after vaccinations.
Therefore, Cadegiani proposed that there could be a loss or malfunction of pancreatic beta cells, as studies have shown that the spike proteins are able to directly affect and damage these beta cells, likely resulting in their death.
The health of sperm relates to overall body health, Australian research has found. ( koya979/Adobe Stock)
Reproductive Organs
The harms of COVID-19 on male reproductive organs are well established.
A study from Thailand shows that in 153 sexually active men, about 64.7 percent experienced erectile dysfunction during COVID-19 infection, with 50 percent persisting in these symptoms three months after recovery.
Erectile dysfunction has been established in research to be due to dysfunctions of the endothelial cells, and the spike proteins impair endothelial cells.
Studies linking COVID-19 and erectile dysfunction have largely blamed it on the virus’s interaction with ACE2 receptors displayed on the surface of endothelial cells. Endothelial cells are abundant in ACE2 receptors, making them one of the most targeted in COVID-19 infections.
A study evaluating adenovirus DNA vaccines shows that cells exposed to the vaccines also produced spike proteins that could interact and bind with ACE2 receptors, suggestive of equal endothelial damage.
Since the vaccine rolled out in 2021, the Centers for Disease Control and Prevention data reported 193 cases of erectile dysfunction following COVID-19 vaccination.
An Israeli study on sperm donations also noticed a reduction of 15 percent in sperm concentration and 22 percent in motile sperm count following COVID-19 mRNA vaccination.
The authors confirmed in a later response (pdf) that the people tested had no underlying health conditions, and therefore, the reduction couldn’t be because of any underlying health conditions that were existent prior to the vaccination.
Although sperm count gradually made a recovery after 145 days, sperm concentration and motility didn’t return to pre-vaccination levels, with unknown long-term effects.
Concerns of reproductive problems have also been reported in women, most particularly after vaccinations rather than after infection.
VAERS data shows that more than 60 percent of adverse event reports came from women, indicating that women are more vulnerable to post-vaccine symptoms.
Dr. Paul Marik, a critical care expert, also observed that women were at a greater risk of presenting with post-vaccine symptoms in the clinic.
During the pandemic, many women reported menstrual abnormalities following vaccination. A study on Middle Eastern women found almost 70 percent of them reporting menstrual irregularities after vaccination.
A study published on the website My Cycle Story reported more than 290 women who have experienced decidual cast shedding after the COVID-19 vaccines rolled out, even though less than 40 such cases have been documented over the past 109 years. This also indicated that many of the reproductive symptoms women were suffering from may be vaccine related, rather than related to COVID-19 infections.
Cadegiani predicted greater adverse events in pregnancies for the coming future.
He cited a study that concluded “no association” between COVID-19 vaccines and fertility. However, the data show that unvaccinated women had a higher rate of pregnancy than the vaccinated, both for clinical and biochemical pregnancy.
The authors of the paper reviewed 10 studies and found that unvaccinated women have a clinical and biochemical pregnancy rate of 47 and 60 percent, respectively, while the vaccinated had a rate of 45 and 51 percent.
Cadegiani predicted more cases of endocrine pathologies as a result of spike injuries in the future.
“Endocrine diseases progress slowly and then only clinically appear in the severe states,” Cadegiani said. “So it’s not possible to tell this [anytime] beforehand.”
Facebook use can both spike and regulate the levels of stress hormone cortisol in teenagers, finds a new study by researchers at University of Montreal, Canada.
Having more than 300 Facebook friends increased teenagers’ levels of cortisol, the study found.
On the other hand, teenagers who act in ways that support their Facebook friends – for example, by liking what they posted or sending them words of encouragement – decreased their levels of cortisol, Techvibes.com reported.
“While other important external factors are also responsible, we estimated that the isolated effect of Facebook on cortisol was around eight percent,a said lead researcher professor Sonia Lupien.
Participants were asked about their frequency of use of Facebook, their number of friends on the social media site, their self-promoting behaviour, and finally, the supporting behaviour they displayed toward their friends.
Along with these four measures, the team collected cortisol samples of the participating adolescents.
“We were able to show that beyond 300 Facebook friends, adolescents showed higher cortisol levels,” Lupien added.
None of the adolescents suffered from depression at the time of the study.
“We did not observe depression in our participants. However, adolescents who present high stress hormone levels do not become depressed immediately. It can occur later on,” Lupien said.
Here’s a mind-bender: Being overweight often has nothing to do with calories or exercise. For a huge number of us, the problem is instead about misfiring hormones. Research is still catching up with this paradigm shift, which has yet to be comprehensively studied. But seeing how this revelation has helped my patients (and me) slim down and feel better gives me confidence that it’s true for most women who are trying to lose weight and can’t. You already know about some weight-affecting hormone issues, like thyroid and insulin imbalances. But other, more subtle ones could also be keeping you from the body you want. Biology class, anyone?
Too Much Leptin Swells Your Appetite
I think of leptin as the hormone that says, “Darling, put down the fork.” Under normal circumstances, it’s released from your fat cells and travels in the blood to your brain, where it signals that you’re full. But leptin’s noble cause has been impeded by our consumption of a type of sugar called fructose, found in fruit and processed foods alike. When you eat small amounts of fructose, you’re OK. But if you eat more than the recommended 5 daily servings of fruit (which in recent decades has been bred to contain more fructose than it used to) plus processed foods with added sugar, your liver can’t deal with the fructose fast enough to use it as fuel. Instead, your body starts converting it into fats, sending them off into the bloodstream as triglycerides and depositing them in the liver and elsewhere in your belly. As more fructose is converted to fat, your levels of leptin increase (because fat produces leptin). And when you have too much of any hormone circulating in your system, your body becomes resistant to its message. With leptin, that means your brain starts to miss the signal that you’re full. You continue to eat, and you keep gaining weight.
The hormoneGLP-1 is released when we eat and makes us feel full or sated toward the end of the meal.
GLP-1 receptors are also activated in parts of the brain that are linked to satisfaction or a sense of reward. This indicates the hormone is directly involved in our experience of gratification.
Scientists reason that by blocking these receptors they can prevent smokers from feeling satisfied after a cigarette.
“Without this kind of reward, a smoker will not keep smoking. It can reduce addiction and the risk of a relapse,” says Elisabet Jerlhag, a researcher at the Sahlgrenska Academy of the University of Gothenburg.
Jerlhag and colleagues have investigated this new potential weapon in the battle against smoking.
Smokers require treatment
The ranks of daily, habitual smokers are on the decline but tobacco smoke remains a substantial public health challenge. One in four Norwegians smoke on occasion and the numbers of such “party smokers” are fairly stable.
Even those who are not heavy, daily smokers can find it hard to stub their cigs for good.
“Nicotine is remarkably habit-forming, and many people find it terribly hard to quit smoking. We need to start accepting dependency as a disorder that requires treatment,” says Jerlhag.
Tested on nicotine mice
To test whether GLP-1 regulates gratification, the researchers experimented with another chemical substance, Exendin-4 (Ex4), which imitates GLP-1’s effect on receptors. The substance was administered to a group of lab mice who had been given doses of nicotine.
The researchers then observed the mice’s movement patterns as well as the dopamine releases in their brains.
They found that nicotine made the mice more active, but the addition of Ex4 reduced that activity. However, mice that had not been given nicotine to start with did not experience the mitigating effect of Ex4. Nicotine increased the release of dopamine in their brains, but this was reduced when Ex4 had been given earlier.
The researchers concluded that GLP-1 receptors regulated the effect of nicotine on the reward functions in the brains of mice, and that Ex4 diminished the effect of nicotine.
Same effect on alcohol, amphetamines and cocaine
The researchers point out that other experiments have shown the same mitigating effect of Ex4 with other habit-forming substances such as alcohol, amphetamines and cocaine.
“Because Ex4 also reduced the motivation for consuming sucrose, this could indicate that GLP-1 receptors play a key role in the gratification created by addictive substances and the rewards of natural activities,” they add.
The researchers believe that substances that mimic the GLP-1 hormone should be considered for new prospective treatment regimens to help battle smoking and nicotine addiction.
Developing new medications
This method, which prevents smoking from soothing the nicotine cravings, is different from existing methods for treating habitual tobacco use, such as nicotine patches, or drugs such as bupropion or varenicline.
The hope is that the findings can lead to the development of new medications that mimic GLP-1. These kind of drugs have already been approved for diabetes, so that it should be relatively easy to get the green light to use them to help smokers kick their habit.
“Rewards are a prime reason why we become addicts. So we think medications that work in the same way as GLP-1 can have a positive impact on nicotine dependency. This is a whole new approach,” Jerlhag says.
John Amory, a doctor at the University of Washington, has been developing a male contraceptive for 15 years. Turns out, it’s harder than it sounds. We spoke with him to find out why.
PopSci: Why is it taking so long to produce a birth-control pill for men?
John Amory:Women make one egg a month, but men make 1,000 sperm every second of every day, from puberty until the day they die. Turning that off is difficult.
JA:If you give a man enough testosterone, the brain will shut down the secretion of gonadotropins, which are the hormones that signal the testes to make sperm. This is why most bodybuilders are infertile, by the way. But it doesn’t work in all men.
PS: How many men does testosterone work for?
JA:We have never been able to get more than 95 percent effectiveness. It’s possible to identify who testosterone won’t work for, but it involves getting a lot of sperm counts. It would be much nicer if you could just say, “Take this and it will work.” Women don’t have to undergo ovulation detections and testing to see if the Pill is going to work for them.
PS: The World Health Organization funded a study across eight countries for hormone-based contraception, but last year, it shut down the study early. What happened?
JA:There were side effects, including severe depression. Some men don’t take hormonal shifts very well.
PS: What other approaches might work?
JA:Sperm have a pretty daunting mission. There’s a lot that can go wrong. Researchers have injected monkeys with eppin, a protein that coats sperm so they can’t swim. There’s also the process by which sperm make energy. If you can block that, you’d get tired sperm. Also, the testes need vitamin A to produce sperm, and there’s an enzyme that converts vitamin A to its active metabolite, retinoic acid. No retinoic acid, no sperm. I’m developing drug inhibitors that stop retinoic-acid production in the testes. I’m hopeful that we’ll have something approved in five years.
PS: Do you expect much demand for the male pill?
JA:Yes. Men are interested in having sex. Most of the time they’re not as interested in fathering a pregnancy.
Researchers think they’ve hit on why a common obesity gene causes weight gain: Those who carry a version of it don’t feel full after eating and take in extra calories. That’s because the variant of the FTOgene in question, which one in six individuals carry, leads to higher levels of ghrelin, a hormone involved in mediating appetite and the body’s response to food, researchers have discovered. While most studies on FTOhave relied on mice, the new work analyzed blood samples and brain scans from humans.
“This is a very exciting piece of research,” says geneticist Andrew Hattersley of the Peninsula Medical School in Exeter, U.K., who was not involved in the new study. “There is a lot of work that’s been done on the mechanism of FTO in animals, but you have to be careful about applying those lessons to people. So it’s nice to finally see work done in humans.”
Hattersley was part of a team that in 2007 reported that people who had one version of the FTOgene, called AA, weighed an average of 3 kilograms more than those with the TT version of the gene. Since then, studies in mice have shown that in everyone, there are high levels of the FTO protein in brain areas that control energy balance. Researchers have also found that animals with the AA version tend to eat more and prefer high-fat food compared with those with the TT version. But why FTO had this effect wasn’t known.
Rachel Batterham, an endocrine and obesity researcher at University College London, thought that gut hormones that mediate the body’s response to eating could be the missing link between FTOand food intake. One such hormone is ghrelin, known to be produced by gut cells to stimulate hunger. So Batterham and her colleagues measured levels of ghrelin in the blood of nonobese men with the AA or TT versions of FTO. In those with the TT variant, ghrelin levels rose before a meal, when the person experienced hunger, and fell after eating, as expected. But in those with the obesity-associated AA version, ghrelin levels stayed relatively high even after eating. Moreover, the AA individuals reported a faster increase in hunger after a test meal. And MRI scans revealed that, when the test subjects were shown images of food before or after eating, brain activity in areas associated with motivation and rewards remained high before and after the meal in AA individuals. This suggests that the increased ghrelin levels were impacting the brain’s response to food—which “fits very well with what we already know the effects of ghrelin,” Batterham says.
But could higher ghrelin levels be unrelated to FTO? The researchers don’t think so, in part because they found that in isolated human cells, increased levels of FTO protein led to more ghrelin production. The reason this happens, the group showed, is because that the FTOprotein actually alters the ghrelin gene, causing methyl chemical groups to be removed, a so-called epigenetic modification that impacts how much protein the ghrelin gene produces. The AA gene variant, the researchers report online today in The Journal of Clinical Investigation, removed more methyl groups from the gene, leading to increased levels of the hunger hormone.
Whether that proves true, the full story is FTOremains to be uncovered, Hattersley says. “What we don’t know is whether FTO is changing many things that alter appetite, of which ghrelin is just one,” he says. “I suspect human appetite and obesity is more complex than a single hormone.”
Neurobiologist Tamas Horvath of Yale University agrees. “This is a beautiful piece of work at face value,” he says. “But I think it’s reasonable to continue pursuing many other avenues to see what else might be going on here.”
A review argues that the hormone oxytocin affects athletic performance, because of its role in modulation of emotional and social processes important to team sports. Jill Jouret reports.
In elite sports, winning can come down to subtle aspects of performance. For example, an individual’s gestures and expressions of emotion can affect team performance and a contest’s outcome. A study of touch behaviour (eg, high-fives, chest bumps) among players in America‘s National Basketball Association showed that teams who touched more had better season records. An investigation of football players’ body language after successful penalty kicks in World Cup and European Championship matches noted that specific celebratory behaviours were associated with the team eventually winning a shootout. Perhaps the emotional display by the elated kicker led to a positive emotion in a teammate, who struck the ball better on his attempt. Whether through touch or emotional expression, trust and goodwill communicated among players motivates the team toward higher achievement.
A review by Gert-Jan Pepping and Erik J Timmermans, published in September, 2012, in The Scientific World Journal, argues for oxytocin as the biochemical basis of such emotion transfer that can lead to enhanced performance in team sports. Via its action as a peripheral hormone and a central neurotransmitter, oxytocin modulates a diverse range of mammalian processes. Peripheral effects include regulation of uterine contraction during labour, stimulation of lactation, and modulation of inflammation. Oxytocin receptors are expressed by neurons in the brain and spinal cord, and it has been shown to affect pair bonding, maternal behaviour, and sexual receptivity. Oxytocin is destroyed in the gastrointestinal tract, and does not seem to cross the blood—brain barrier when given intravenously, so its effects are studied in animals by injection of a synthetic form directly into the brain, and in humans via administration of a nasal spray.
Oxytocin is often referred to as the feel-good hormone, because it is released in response to touch and is associated with feelings of calmness and stress reduction. A positive feedback loop means that higher oxytocin concentrations further increase the desire for tactile interaction. This association seems to be the basis for its role in promotion of mother—child bonds and fidelity in monogamous pairs. A study in the Journal of Neuroscience provided behavioural evidence of oxytocin’s involvement in maintenance of bonds among committed couples. After administration of intranasal oxytocin, men in monogamous relationships kept a greater distance between themselves and an attractive researcher than did those given placebo, and approached an attractive image more slowly, whereas no such effect was seen with single men. No wonder oxytocin is also known as the love hormone.
In their review, Pepping and Timmermans outline the argument for giving oxytocin yet a third moniker—the sports hormone. Positive emotions and prosocial behaviour are associated with improved performance in achievement settings in general, hence increasing investment in work environments that enhance team spirit and boost individual motivation. In sports, emotional expressions underpin the continuing exchange of information and mood between teammates and opponents. An emotional display by one player can inspire a similar mood in teammates, and the team’s overall disposition can motivate individual performance. This convergence of mood, or emotional contagion, is a key element in team unity. Measuring a player’s hormone levels during competition is a logistical challenge, but the studies reviewed by Pepping and Timmermans show that, in controlled settings, oxytocin affects processes central to emotional contagion and social perception.
Empathy denotes cognitive ability to adopt another person’s point of view, or emotional capacity to have a shared feeling on the basis of another person’s experience. Cognitive empathy is an important quality for an athlete, since it allows them to understand and predict other players’ behaviour, and emotional empathy contributes to convergence of mood (and motivation) among teammates. The Multifaceted Empathy Test is used to measure empathy, by asking study participants to rate emotional reactions to pictorial stimuli; those given one dose of intranasal oxytocin before the test reported higher empathy than those given placebo. Intranasal oxytocin also improved performance on the Reading the Mind in the Eyes Test, which measures participants’ ability to infer a mental state from subtle facial cues.
Reading emotions such as fear or determination in other players can help athletes make quick decisions about their own actions, and oxytocin seems to be a key biological component for processing these social cues. Pepping and Timmermans describe a study in which MRI showed higher brain activity in specific regions associated with emotion recognition when participants given oxytoxin (vs placebo) were shown images of facial expressions. One dose of oxytocin also improved recognition (ie, at lower intensities) of an emotion emerging on a dynamic, computer-generated face that started with a neutral expression.
Studies showing an effect of oxytocin on gaze behaviour suggest a mechanism for how it modulates emotion recognition, and provide further evidence of its involvement in social exchanges. Tracking the eye movements of men given intranasal oxytocin (vs placebo) showed longer gaze duration and fixation on the eye region of neutral faces. Eyes are the main source of information in interpersonal communication, and gaze behaviour is central to impression-forming among athletes. Sports psychologists have studied gaze behaviour in the context of football penalty kicks, to define the best kicking strategy (eg, to look or not to look at the target), but from a goalkeeper’s point of view, kickers who gaze directly at them for longer create a more imposing impression. To the extent that oxytocin is involved in detection of confidence or fear, a boost in either party could make the difference.
At the elite level, in which superior talent is universal (and modesty in interviews is advised), team unity is often credited for a win. Trust, generosity, and cooperation are indispensable processes for building and maintaining team cohesion, and according to Pepping and Timmermans, oxytocin is once again involved. In games with monetary stakes, individuals given oxytocin make trusting decisions more often than those given placebo. People are also more generous under the influence of oxytocin; when asked to make a masked, one-sided decision on how to split a sum of money with a stranger, a group given oxytocin was 80% more generous than those given placebo. Oxytocin enhanced cooperative decision making when participants played games with economic incentives to cooperate. Stronger incentives lead to greater cooperation, but only if social information was present. When social information was absent, players who received oxytocin were actually less cooperative, which suggests that the oxytocin system intricately modulates risk-taking and risk-aversion in social exchanges.
With so much evidence for oxytocin’s role in athletic performance, particularly in the context of team sports, will players be stashing oxytocin inhalers into their equipment bags for a quick hit mid-game? Pepping and Timmermans point out that oxytocin’s effects are not universally prosocial. Compared with placebo, oxytocin administration increased ratings of envy (ie, a negative emotional reaction to another player’s good fortune) and gloating (ie, malicious pleasure at another’s misfortune) in economic games designed to elicit these negative social emotions. Athletic pursuits are awash with relative gain and loss situations, and keeping composure is important for success, so an artificial boost of oxytocin could be ill advised.
As professional cycling joins the rogue’s gallery of sporting doping scandals, talk of another performance-enhancing drug might seem distasteful. But research suggests that there are subtle ways to improve ability through the natural stimulation of oxytocin, which will always be legal. The high-five, the fist-pump, and the group hug remain staple elements of sporting life, and dosing up on a little more might just make the difference between winners and losers.
A review argues that the hormone oxytocin affects athletic performance, because of its role in modulation of emotional and social processes important to team sports. Jill Jouret reports.
In elite sports, winning can come down to subtle aspects of performance. For example, an individual’s gestures and expressions of emotion can affect team performance and a contest’s outcome. A study of touch behaviour (eg, high-fives, chest bumps) among players in America‘s National Basketball Association showed that teams who touched more had better season records. An investigation of football players’ body language after successful penalty kicks in World Cup and European Championship matches noted that specific celebratory behaviours were associated with the team eventually winning a shootout. Perhaps the emotional display by the elated kicker led to a positive emotion in a teammate, who struck the ball better on his attempt. Whether through touch or emotional expression, trust and goodwill communicated among players motivates the team toward higher achievement.
A review by Gert-Jan Pepping and Erik J Timmermans, published in September, 2012, in The Scientific World Journal,argues for oxytocin as the biochemical basis of such emotion transfer that can lead to enhanced performance in team sports. Via its action as a peripheral hormone and a central neurotransmitter, oxytocin modulates a diverse range of mammalian processes. Peripheral effects include regulation of uterine contraction during labour, stimulation of lactation, and modulation of inflammation. Oxytocin receptors are expressed by neurons in the brain and spinal cord, and it has been shown to affect pair bonding, maternal behaviour, and sexual receptivity. Oxytocin is destroyed in the gastrointestinal tract, and does not seem to cross the blood—brain barrier when given intravenously, so its effects are studied in animals by injection of a synthetic form directly into the brain, and in humans via administration of a nasal spray.
Oxytocin is often referred to as the feel-good hormone, because it is released in response to touch and is associated with feelings of calmness and stress reduction. A positive feedback loop means that higher oxytocin concentrations further increase the desire for tactile interaction. This association seems to be the basis for its role in promotion of mother—child bonds and fidelity in monogamous pairs. A study in the Journal of Neuroscience provided behavioural evidence of oxytocin’s involvement in maintenance of bonds among committed couples. After administration of intranasal oxytocin, men in monogamous relationships kept a greater distance between themselves and an attractive researcher than did those given placebo, and approached an attractive image more slowly, whereas no such effect was seen with single men. No wonder oxytocin is also known as the love hormone.
In their review, Pepping and Timmermans outline the argument for giving oxytocin yet a third moniker—the sports hormone. Positive emotions and prosocial behaviour are associated with improved performance in achievement settings in general, hence increasing investment in work environments that enhance team spirit and boost individual motivation. In sports, emotional expressions underpin the continuing exchange of information and mood between teammates and opponents. An emotional display by one player can inspire a similar mood in teammates, and the team’s overall disposition can motivate individual performance. This convergence of mood, or emotional contagion, is a key element in team unity. Measuring a player’s hormone levels during competition is a logistical challenge, but the studies reviewed by Pepping and Timmermans show that, in controlled settings, oxytocin affects processes central to emotional contagion and social perception.
Empathy denotes cognitive ability to adopt another person’s point of view, or emotional capacity to have a shared feeling on the basis of another person’s experience. Cognitive empathy is an important quality for an athlete, since it allows them to understand and predict other players’ behaviour, and emotional empathy contributes to convergence of mood (and motivation) among teammates. The Multifaceted Empathy Test is used to measure empathy, by asking study participants to rate emotional reactions to pictorial stimuli; those given one dose of intranasal oxytocin before the test reported higher empathy than those given placebo. Intranasal oxytocin also improved performance on the Reading the Mind in the Eyes Test, which measures participants’ ability to infer a mental state from subtle facial cues.
Reading emotions such as fear or determination in other players can help athletes make quick decisions about their own actions, and oxytocin seems to be a key biological component for processing these social cues. Pepping and Timmermans describe a study in which MRI showed higher brain activity in specific regions associated with emotion recognition when participants given oxytoxin (vs placebo) were shown images of facial expressions. One dose of oxytocin also improved recognition (ie, at lower intensities) of an emotion emerging on a dynamic, computer-generated face that started with a neutral expression.
Studies showing an effect of oxytocin on gaze behaviour suggest a mechanism for how it modulates emotion recognition, and provide further evidence of its involvement in social exchanges. Tracking the eye movements of men given intranasal oxytocin (vs placebo) showed longer gaze duration and fixation on the eye region of neutral faces. Eyes are the main source of information in interpersonal communication, and gaze behaviour is central to impression-forming among athletes. Sports psychologists have studied gaze behaviour in the context of football penalty kicks, to define the best kicking strategy (eg, to look or not to look at the target), but from a goalkeeper’s point of view, kickers who gaze directly at them for longer create a more imposing impression. To the extent that oxytocin is involved in detection of confidence or fear, a boost in either party could make the difference.
At the elite level, in which superior talent is universal (and modesty in interviews is advised), team unity is often credited for a win. Trust, generosity, and cooperation are indispensable processes for building and maintaining team cohesion, and according to Pepping and Timmermans, oxytocin is once again involved. In games with monetary stakes, individuals given oxytocin make trusting decisions more often than those given placebo. People are also more generous under the influence of oxytocin; when asked to make a masked, one-sided decision on how to split a sum of money with a stranger, a group given oxytocin was 80% more generous than those given placebo. Oxytocin enhanced cooperative decision making when participants played games with economic incentives to cooperate. Stronger incentives lead to greater cooperation, but only if social information was present. When social information was absent, players who received oxytocin were actually less cooperative, which suggests that the oxytocin system intricately modulates risk-taking and risk-aversion in social exchanges.
With so much evidence for oxytocin’s role in athletic performance, particularly in the context of team sports, will players be stashing oxytocin inhalers into their equipment bags for a quick hit mid-game? Pepping and Timmermans point out that oxytocin’s effects are not universally prosocial. Compared with placebo, oxytocin administration increased ratings of envy (ie, a negative emotional reaction to another player’s good fortune) and gloating (ie, malicious pleasure at another’s misfortune) in economic games designed to elicit these negative social emotions. Athletic pursuits are awash with relative gain and loss situations, and keeping composure is important for success, so an artificial boost of oxytocin could be ill advised.
As professional cycling joins the rogue’s gallery of sporting doping scandals, talk of another performance-enhancing drug might seem distasteful. But research suggests that there are subtle ways to improve ability through the natural stimulation of oxytocin, which will always be legal. The high-five, the fist-pump, and the group hug remain staple elements of sporting life, and dosing up on a little more might just make the difference between winners and losers.
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