Exercise is good for you

Exercise changes the way our bodies work at a molecular level

9 May, 2017

By Andrew Thomas
NYR Natural News

Exercise is good for you, this we know. It helps build muscle, burn fat and make us all into happier, healthier people. But long before you start looking the way you want, there are other hidden, more immediate, molecular and immunological changes taking place inside your cells. Changes which could be responsible for protecting us from heart disease, high blood pressure, type 2 diabetes – and even stave off old age and cancer

You may think that “molecular” changes may not be that much of a big deal. Surely it is fat loss and muscle gain that are the best outcomes of exercise? Actually, molecular changes affect the way genes and proteins are controlled inside cells. Genes can become more or less active, while proteins can be rapidly modified to function differently and carry out tasks such as moving glucose into cells more efficiently or protect cells from harmful toxins.

Type 2 diabetes causes all kinds of health problems, including cardiovascular disease, high blood pressure, blindness, kidney failure and nerve damage, and may lead to limb amputation. The underlying cause is the development of a heightened inflammatory state in the body’s tissue and cells. This damages cells and can eventually lead to insulin resistance and, ultimately, type 2 diabetes.

The main risk factors for type 2 diabetes include obesity, a poor diet and a sedentary lifestyle. However, we have found that even low-intensity exercise, such as brisk walking, can increase the body’s insulin sensitivity. This means that people at risk of developing diabetes become less prone because they are able to metabolise glucose more efficiently.

In our study, we asked 20 sedentary people who were at risk of developing diabetes to walk briskly for 45 minutes, three times a week, for eight weeks. Although there was no change in their weight, blood pressure or cholesterol level, on average each participant lost a significant six centimetres from their waist circumference. And, more importantly, there was a reduction in their diabetic risk.

Immune system benefits

Interestingly, there were also exercise-induced changes in the participants’ monocytes – an important immune cell that circulates in the bloodstream. This led to a reduction in the body’s inflammatory state, one of the main risks for type 2 diabetes.

When our body is under attack from foreign invaders such as microbes, immune cells such as monocytes change into “microbe-eating” macrophages. Their main function is to fight infection in our tissues and lungs. There are two main types of macrophages, M1 and M2. M1 macrophages are associated with pro-inflammatory responses and are necessary for aggressively fighting off infections. However, in obese people who do not exercise, these cells become active even in the absence of infection. This can lead to an unwanted, heightened inflammatory condition which may “trigger” diabetes.

On the other hand, M2 macrophages play a role in “switching-off” inflammation and are instrumental in "damping down" the more aggressive M1s. So a healthy balance of M1 and M2 macrophages is crucial to maintaining an optimal immune response to fighting infections – and it may help prevent the heightened inflammatory condition which comes from a lack of exercise and obesity too.

Other studies have also shown that exercise has a beneficial impact on tissues’ immune cell function and can reduce unnecessary inflammation. Exercise training in obese individuals has been found to reduce the level of tissue inflammation specifically because there are fewer macrophage cells present in fat tissue.

In addition, researchers have found a significant link between exercise and the balance of M1 and M2 macrophages. It has been shown that acute exercise in obese rats resulted in a shift from the “aggressive” M1 macrophages to the more “passive” M2 and that this reduction in the inflammatory state correlated with an improvement in insulin resistance.

Time to move

There is no definitive answer as to how much and what intensity of exercise is necessary to protect us from diabetes. Though some researchers have shown that while higher-intensity exercise improves overall fitness, there is little difference between high and low-intensity exercise in improving insulin sensitivity.  However, a new study has found that all forms of aerobic exercise – in particular, high-intensity interval training such as cycling and running – can effectively stop ageing at the cellular level. The exercise caused cells to make more proteins for their energy-producing mitochondria and their protein-building ribosomes. Researchers also observed that these “molecular” changes occurring at the gene and protein levels happened very quickly after exercise and that the effects prevented damage to important proteins in the cells and improve the way in which insulin functions.

Although you might not see the changes you want immediately, even gentle exercise can make a big difference to the way the body’s cells behave. This means that exercise could have far-reaching health benefits for other inflammatory associated diseases and possibly protect us against ageing and cancer too.

FISH OIL (KRILL OIL) COMPONENT HELPS DAMAGED BRAIN, RETINA CELLS SURVIVE, SHOWS RESEARCH

Fish oil (Krill Oil) component helps damaged brain, retina cells survive, shows research

April 21, 2017 Louisiana State University Health Sciences Center - fish oil.

NDP1, a signaling molecule made from DHA, can trigger the production of a protective protein against toxic free radicals and injury in the brain and retina, research shows for the first time.

A team of researchers led by Nicolas Bazan, MD, PhD, Boyd Professor and Director of the Neuroscience Center of Excellence at LSU Health New Orleans School of Medicine, has shown for the first time that NDP1, a signaling molecule made from DHA, can trigger the production of a protective protein against toxic free radicals and injury in the brain and retina. The research, conducted in an experimental model of ischemic stroke and human retinal pigment epithelial (RPE) cells, is available in Advance Publication Online in Nature Research's Cell Death and Differentiation.

Neuroprotectin D1 (NPD1) is a lipid messenger made from the omega-3 fatty acid docosahexaenoic acid (DHA) made on demand when cell survival is compromised. NPD1 was discovered and named in 2004 by Dr. Bazan and colleagues. Oxidative stress, resulting from the constant production of damaging free radicals, lays the groundwork for cell death. Cell death is accelerated by catastrophic events, like ischemic stroke, as well as neurodegenerative and blinding-eye diseases. The research team found that when systematically administered one hour after two hours of experimental stroke, NPD1 increased the production and availability of ring finger protein 146, which has been named Iduna. Iduna facilitates DNA repair and protects against a form of programmed cell death in stroke known as parthanatos by suppressing the production of a destructive protein called PARP. Their findings also include that NDP1 enhanced the production of Iduna and protection in two types of human RPE cells (ARPE-19 and primary RPE) undergoing uncompensated oxidative stress. The researchers found that the effect of NDP1 on Iduna activity peaked at six hours after the onset of the oxidative stress, A dose-dependent curve showed an increase of Iduna activity starting as 25 nM NPD1 in both types of human RPE cells. These results suggest that NDP1 selectively induces Iduna activity when uncompensated oxidative stress triggers the formation of NPD1 that in turn activates Iduna.

"These findings are significant because they show how NPD1, a lipid mediator made 'on demand,' modulates the abundance of a critically important protein (Iduna) toward cell survival," notes Nicolas Bazan, MD, PhD, Boyd Professor and Director of the Neuroscience Center of Excellence at LSU Health New Orleans School of Medicine. "This protein, relatively little studied, turns out to be key for cell functional re-programing and subsistence." DHA, found in fish oil, is an essential omega-3 fatty acid and is vital for proper brain function. It is also necessary for the development of the nervous system, including vision. A study from the Bazan laboratory published in 2011 found that DHA triggered the production of Neuroprotectin D1, a naturally occurring neuroprotective molecule in the brain derived from DHA. NDP1 bioactivity governs key gene interactions decisive in cell survival when threatened by disease or injury.

"The further unraveling of the molecular details of DHA-NPD1-Iduna expression signaling may contribute to possible therapeutic interventions for retinal degenerations and ischemic stroke." says Bazan.

Louisiana State University Health Sciences Center. "Fish oil component helps damaged brain, retina cells survive, shows research." ScienceDaily. ScienceDaily, 21 April 2017.