Dr Peter Richard Pedersen

Research, Articles, Case Histories and Plausable Theories in Support of Health and Longevity... naturally

Dr Peter Richard Pedersen DC DO NTMD CIM CDN

Graduate - Sydney College of Osteopathy - Sydney College of Chiropractic
International College of Applied Kinesiology
Member Chiropractic & Osteopathic College of Australasia (COCA)

OSTEOPATH, CHIROPRACTOR, TRADITIONAL & INTEGRATIVE MEDICINE
Myofascial Trigger Point Dry Needling Neuromuscular Procedures, Biopuncture
Non-Surgical Solutions for Tendinopathy, Tenosynovitis, Bursitis & Knee Cartilage

Ageing is a process of gradual maturation. Senescence is the process by which the capacity for cell division and the capacity for growth and function are lost over time, ultimately leading to death.


Ageing is thought to have the positive component of development (eg, increased wisdom, experience, and expertise) and the negative component of decline. The term senescence is the most common term for the decline component and refers only to changes that are deleterious.
The changes that occur with ageing can be categorized as those that result from ageing itself and those that result from diseases, lifestyle, and exposures. Normal ageing is sometimes used to refer to changes attributed to ageing itself. Usual ageing (sometimes also but confusingly referred to as normal aging) refers to the common complex of diseases and impairments that occur in many elderly people. However, this complex is hard to define because people age very differently: Some acquire diseases and impairments, and others seem to escape disease altogether and are said to have died of "old age."

 

Some animals, including certain birds and fish, do not appear to age at all. Successful (healthy) ageing refers to a process by which deleterious effects are minimized, preserving function until senescence makes continued life impossible. People who age successfully avoid experiencing many of the undesirable features of ageing and, whether they have a disease or not, remain functional both physically and mentally.


The percentage of community-dwelling people > 65 who report needing assistance with activities of daily living has decreased over the last 2 decades, as has the percentage of people with debilitating disease. One viable explanation for these changes is an increase in the percentage of people who are ageing successfully, although there may be other explanations.


Disease vs ageing:

 

With ageing, many physiologic functions decline. Many of these declines are attributed to ageing itself; in other words, they are considered normal, not disease-related. The distinction between normal and disease-related may be clear or may simply be defined by statistical distribution. With presbyopia (decreased accommodation of the lens of the eye), the distinction seems clear because presbyopia occurs in virtually all elderly people and no cause or explanation has been identified other than ageing itself. However, with glucose control and cognition, statistical distribution may define the distinction between normal and disease-related. Some degree of glucose intolerance is considered part of normal ageing, but diabetes, although very common, is considered a disease. Cognitive decline is nearly universal with ageing and is considered normal ageing; however, dementia, although common in late life, is considered a disease.

 

Anti-ageing:

 

There has always been conversation about "The Fountain of Youth", reputed miracle waters, tonics, elixers or therapies that can reverse, (we would settle for slow down), the ageing process. Is there anything that we can do or is the decline into decrepitude inevitable and unalterable?

 

GOOD NEWS

 

Researchers have identified anti-ageing enzymes in the body...one in particular has been investigated by Prof David Sinclair, of the University of NSW Medicine, which has the potential to prevent age related diseases such as cancer, Alzheimer's and type-2 diabetes, while also extending life spans. The antioxidant enzyme, catalase, has been shown to increase the lifespan of (good old laboratory) mice by 18.5%...that would add 18 years to an average human lifespan.

 

Medical research is skewed towards pharmacology, but we can use the vast medical resources to further our knowledge and application of natural healthcare. Harvard University researchers confirm that antioxidants (and related substances) provide" protection against many of the scourges of ageing", and say there is abundant evidence of the health benefits of eating whole fruits, vegetables, wholegrains, legumes and nuts...but the use of antioxidant supplements is not, as yet, advocated by the (strict) medical science community.

 

"CALERIE" Comprehensive Assessment of Long-term Effects of Reducing Intake Of Energy. (A Recent Study)

 

Calorie Restriction and short-term fasting are proven methods of improving measurable health parameters...insulin levels, core body temperature, cortisol levels, inflammation and markers of ageing. This requires a reduction in calorie consumption of 20 to 30%. Popularly called "Intermittant Fasting", reduced meal frequency is relatively painless, requiring two non-consecutive days of reduced eating each week. No junk food, sugar or alcohol on those days...the benefits appear to be disproportionate to the effort. According to one popular author, reversing type-2 diabetes, reducing joint inflammation and allergic reactions.

 

It’s indisputable—exercise is good for you. But on a molecular level, scientists don’t really know why. Published Jan 18, 2012, in Nature, researchers show for the first time that a cellular housekeeping mechanism, called autophagy, could be the source of the beneficial effects of exercise, including protection against diabetes. Targeting the pathway could mimic the health effects of exercise—all the perks with none of the sweat—and help treat type II diabetes, the authors suggest.

“It’s really a new idea,” said Marc Francaux, who studies the biochemistry of exercise at the Université catholique de Louvain and was not involved in the research. “They use three different transgenic mouse models. It’s really convincing.”

“It provides a fresh look into how exercise produces its benefits,” said Gökhan Hotamisligil, who studies metabolic regulatory pathways at the Harvard School of Public Health and also did not participate in the study. “It’s an important and convincing article.”

Autophagy is an internal recycling system that degrades damaged or unwanted organelles and proteins in a cell and produces energy. In animal models, this process has been shown to protect against cancer, neurodegenerative disorders, infections, diabetes, and more. “Exercise is known to protect against all these same diseases,” said Beth Levine, a biologist at the University of Texas Southwestern Medical Center, “so it made sense to us that exercise might induce autophagy.”

 

Levine and her team assessed the protective effects of exercise in mice fed a high fat diet to induce diabetes. Normally during exercise, blood glucose levels decrease and the animal becomes more sensitive to insulin, so that low or normal levels of insulin are sufficient to maintain healthy blood glucose levels and prevent diabetes. “We postulated that autophagy is necessary for these protective effects of exercise,” said Levine. When placed on the high fat diet, both the mice gained weight and showed impaired insulin sensitivity, a hallmark of type II diabetes. Running on a treadmill improved these symptoms in animals capable of exercise-induced autophagy.

 

Her team next plans to investigate the role of autophagy in other diseases in which exercise has beneficial effects, such as cancer and Alzheimer’s.

Another surprising result from the study was the evidence that autophagy is activated during exercise in the liver and pancreas—tissues other than skeletal and cardiac muscle. “The entire field has been focused on benefits of exercise coming from things that happen in muscle,” said Hotamisligil. “This suggests that certain pathways engaged by exercise extend beyond muscle tissue and influence other metabolically critical sites.”

C. He, et al., “Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis,” Nature, 481:511-5, 2012.

 

 

 

Article by Dr Peter Richard Pedersen

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