Could Sunlight Aid Weight Loss?

Nayak et al. have recently published the findings of their fascinating research into the effects of light on fat metabolism in mice.

Animals have adapted to use light in various ways. The most obvious is our sense of sight – it creates images in the brain through the detection of photons by light sensitive proteins (opsins) in the retina. But there are also non-visual ocular photoreceptors that help regulate our circadian rhythms (body clock), pupillary light reflex and eye development. Interestingly, light sensitive proteins are also found outside the eye. Opsins in our skin can regulate the circadian clock and others can influence blood vessel dilation. In birds, it’s photoreceptors deep within the brain that regulate seasonal breeding behaviour.

There have been suggestions that adipocyte (fat cell) function may be modulated by light. White fat (WAT) acts as a storage site whereas brown fat (BAT) generates heat through a process called non-shivering thermogenesis (NST). During lipolysis, white fat can be broken down into free fatty acids (FFAs) and glycerol. The brown fat can then use the FFAs to generate heat by oxidation. This process plays a crucial role in the regulation of body temperature during cold exposure.

In the current study, Nayak et al. found that lipolysis was brought about by the exposure of light receptors within white fat (encephalopsin, OPN3) to light. OPN3 was particularly sensitive to blue light. The mice lacking OPN3 or light exposure had diminished heat-generating responses when placed in cold environments. The authors conclude: “If the light-OPN3 adipocyte pathways exist in humans, there are potentially broad implications for human health. Our modern lifestyle subjects us to unnatural lighting spectra, exposure to light at night, shift work, and jet lag, all of which result in metabolic disruption. Based on the current findings, it is possible that insufficient stimulation of light-OPN3 adipocyte pathway is part of an explanation for the prevalence of metabolic deregulation in industrialized nations where unnatural lighting has become the norm.”

“Keep your eye fixed on the way to the top,

but don’t forget to look right in front of you.

The last step depends on the first.

Don’t think you’re there just because you see the summit.

Watch your footing,

be sure of the next step,

but don’t let that distract you from the highest goal.

The first step depends on the last.”

René Daumal

Soft Drinks May Cause Menopausal Hip Fractures

A study published this month in the journal Menopause looked into the relationships between carbonated soft drink consumption, osteoporosis (hip and lumbar spine) and incidental hip fractures. For almost 12 years Kremer et al. followed over 72,000 postmenopausal women from the Women’s Health Initiative Observational Study.

The results showed no associations between soft drink consumption and hip or lumbar spine bone mineral density – this finding was in contradiction with previous studies that had found an association. Consuming at least 14 carbonated soft drinks per week was associated with incident hip fractures. The relationship was statistically significant for caffeine-free soft drinks but not for caffeinated soft drinks. Interestingly, there was no significant risk if the intake was less than 14 servings per week, suggesting a ‘threshold effect’ rather than a ‘linear dose-response’ relationship. Drinking more than 14 carbonated soft drinks (non-caffeinated) per week led to a 32% increase in risk of hip fracture compared to women that didn’t drink any soft drinks.

The authors postulate that added sugars may have “a negative impact on mineral homeostasis and calcium balance“. Also, the carbonation of soft drinks “results in the formation of carbonic acid that might alter gastric acidity and, consequently, nutrient absorption“.

Excess Dietary Salt Leads To Cognitive Impairment

Faraco et al. recently discovered mechanisms by which salt-rich diets can lead to cognitive dysfunction in mice. An increase in dietary salt led to a deficiency of nitric oxide in cerebral blood vessels. As nitric oxide is a vasodilator, the reduced levels resulted in decreased cerebral blood flow. In addition, nitric oxide deficiency causes the distortion of a brain protein (tau) which affects the structure and function of nerve cells. The authors conclude that the “avoidance of excessive salt intake and maintenance of vascular health may help stave off the vascular and neurodegenerative pathologies that underlie dementia in the elderly.”

Loving-Kindness Meditation Slows Aging

A recent study by Le Nguyen et al. published in Psychoneuroendocrinology has looked at the effect of loving-kindness meditation on telomore length. Loving-Kindness is a Buddhist meditation that focuses on sending good wishes and kindness to ourselves and others by silently repeating a series of mantras. Telomeres sit at the end of chromosomes and protect the chromosomes from deterioration. Our telomeres gradually shorten over time and this is believed to contribute to aging.

The researchers randomised 142 middle-aged adults into 3 groups: a waiting list control group, a mindfulness meditation group and a loving-kindness meditation group. Telomere length was measured 2 weeks prior to the start and 3 weeks after the end of the 6-week meditation workshop. The results showed that there was significantly less telomere attrition in the loving-kindness meditation group than the control group. The mindfulness meditation group had results that were in between the other 2 groups without being statistically significantly different from either.

We can infer that loving-kindness meditation can slow aging by decreasing the rate at which our telomeres shorten.

Meditation and the Brain

Meditation can be defined as “a family of mental training practices aimed at monitoring and regulating attention, perception, emotion and physiology” (Fox and Cahn, 2019). As with other forms of learning, meditation has the potential to change the brain (neuroplasticity). Fox and Cahn (2019) reviewed decades of meditation research in a paper entitled “Meditation and the brain in health and disease”. Here are some of their findings. The table below summarises the areas of the brain that have been implicated in meditation.

Although “psychologically distinct meditation practices show correspondingly diverse neural correlates”, most practices modulate activity in the insula. Given that awareness of breathing or other body sensations is central to most forms of meditation, and the insula’s role in the awareness of the internal environment, it’s not surprising that meditation leads to a change in structure and function of the insula.

Some interesting discoveries have been made regarding pain. The experience of pain is the combination of the purely sensory aspect of pain with feelings of distress, thoughts relating the pain to the self and various negative emotional interpretations of the experience. “These cognitive-affective elaborations appear to be dissociable from, and temporarily subsequent to, the purely sensory aspects of pain – and what’s more, they may contribute significantly to the subjectively experienced unpleasantness of nociceptive experience (Rainville et al., 1997)”. Meditators were found to have lower pain sensitivity. This may be due to their decreased functional connectivity between primary sensory pain areas and secondary affective-elaborative areas. This supports the idea that seasoned meditators remain focussed on purely sensory aspects of pain whereas non-meditators dwell on emotional and cognitive associations of pain.

Other fascinating discoveries are the impact of meditation on aging. There is usually a decrease in function (glucose metabolism) and structure (amount and density of grey matter) of the brain with aging. However, studies show that meditation may help stave off the effects of aging. In fact, some studies have found no age-related decline in function and/or structure!

But, the limitations of current research must be acknowledged:

• It’s a new field of inquiry
• Agreement amongst researchers is the exception rather than the norm
• Few studies control for factors that may exist between meditators and controls e.g. Diet, stress, sleep, personality, etc.
• Publication bias (the preferential publication of only positive studies)

Paleo Diet May Be Bad For Cardiovascular Health

Research published earlier this month in the European Journal of Nutrition questions the health benefits of the Paleolithic diet. The Paleo diet claims to mimic the diet of our ancestors. It’s high in meat, fruits, vegetables, nuts and seeds but avoids dairy, legumes and grains.

Genoni et al. studied a group of about 100 people over a year. Half the group followed a Paleo diet and the rest followed a diet typical of national recommendations. The authors found that there was a significant difference in the gut bacteria between groups, with an increased presence of Hungatella in the paleo group. Hungatella produces trimethylamine-N-oxide (TMAO), a gut-derived metabolite associated with cardiovascular disease. Consequently the levels of TMAO were higher in the Paleo group and this was inversely associated with whole grain intake.

The authors conclude that “although the Paleo diet is promoted for improved gut health, results indicate long-term adherence is associated with different gut microbiota and increased TMAO. A variety of fiber components, including whole grain sources may be required to maintain gut and cardiovascular health.”

Vagus Nerve Stimulation Reduces Rheumatoid Arthritis Symptoms

Genovese et al. recently presented the results of their research at the Annual European Congress of Rheumatology. They implanted mini neurostimulators in 14 rheumatoid arthritis (RA) patients that had failed to respond to anti-rheumatic medication. In the treatment groups, the vagus nerve was stimulated daily for 12 weeks. The results showed that stimulation of the vagus nerve reduced signs and symptoms of RA as well as decreasing by 30% the levels of cytokines (inflammatory mediators).

The vagus nerve is known to have anti-inflammatory effects and can also be stimulated by less invasive methods such as meditation, breathing exercises, relaxation techniques and acupuncture.

Atherosclerosis and Low Back Pain

Atherosclerosis is well-known for its role in the development of coronary heart disease and stroke. The vascular occlusion that it causes leads to the infarction of heart and brain tissue. But coronary and cerebral blood vessels are by no means the only vessels that become clogged by atheromatous plaques. In 1993, Kauppila et al., from the department of forensic medicine at Helsinki University, postulated that insufficient arterial blood flow may play a role in low back pain. Their post-mortem angiographic study found that, compared to controls, significantly more people with a history of low back pain had anomalies in the arteries that supplied the lumbar spine – the arteries were narrowed by atheromatous lesions and some were completely missing.

Since that landmark study, several cadaver and clinical studies have corroborated the link between stenosis (and occlusion) of the lumbar arteries and the presence of low back pain. In fact, many studies have found an association between the aforementioned lumbar vascular insufficiency and degeneration of the corresponding lumbar discs. This shouldn’t be a surprise because, as Kauppila states, “the disc is located at the end of the nutrient chain, making it one of the first structures to suffer during insufficient nutrient supply.”

In epidemiological studies, associations between cardiovascular risk factors and low back pain (or disc degeneration) are weaker and conflicting. Nevertheless, several studies have linked high blood cholesterol and smoking with low back pain and disc degeneration. It’s important to remember that correlation is different from causation and more research is needed to determine a cause and effect relationship. So, a healthy diet and abstinence from smoking may play a role in the prevention and treatment of low back pain. Further still, and this is pure conjecture on my part, they may have a role to play in maintaining the health of all poorly vascularised tissues (spinal discs, tendons, articular cartilage of joints, etc.).

High Cholesterol Can Cause Tendon Pathology

A recent literature review by Yang et al. suggests that high blood cholesterol is a risk factor in the development and progression of tendon pathology. They found that cholesterol levels were directly correlated with the severity of tendon problems. There is evidence that elevated cholesterol levels lead to inflammatory, structural and mechanical changes in tendons which predispose patients with high cholesterol levels to an increased risk of developing tendinopathies.