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Rejuvenation – forever young?

Halting the ageing process with holistic regulation of the psychological-spiritual-mental and physical processes, along with alteration to lifestyle is one of INAKARB’s essential tasks.

CAUSES OF AGEING – WHY DO WE AGE?

Average life expectancy has significantly increased in recent years in first-world countries. The maximum age which can be achieved seems to have remained constant at approx. 120 years for some time now. The bible mentions that numerous people achieved an age of 80 back then. Today, only about 50% of people reach the age of 80. Only 1% live to be 100 years old.

One might actually think that single-cell organisms cannot die as they reproduce through division. However, they are not immortal as they forfeit their individual existence during the process of division. He-La cells (epithelial cells of a cervical carcinoma from a woman named Henrietta Lacks) are regarded as being immortal. Whether there are actually multicellular “immortal” organisms is not certain.

There are approx. 300 different theories on ageing. There are two principle types of theory as to how ageing develops: theories of genetic causes (programming) and the so-called wear-and-tear theories. The first theories are attributed to about 70% of the causes of ageing and about 30% to the other causes.

PROGRAMME THEORIES – GENETIC CAUSES AND TELOMERE LOSS

Telomere loss theory:

Connective tissue cells are only able to divide approx. fifty times. This corresponds to the so-called Hayflick limit, named after Leonard Hayflick who first observed this during the 1960s. In in-vitro trials (Wright and Shay) with the telomerase enzyme were able to break through the Hayflick limit. Telomerase influences the telomeres – the shortening of chromosome endings which occurs with each cell division. This is not the case for germ cells and blood stem cells. At birth, our telomeres are the length of approx. 10,000 base pairs. At the age of 100, they only measure approx. 5,000 base pairs. Tumour cells appear to be able to prevent this telomere loss with each cell division. Telomerase activity was observed in approx. 90% of these cells.
Wear and tear theories:

1. Free radicals:

Ageing as a result of pineal gland failure. Melatonin as an “anti-ageing” hormone. The degree of calcification of the pineal gland determines the ability of the gland to produce melatonin (Reiter RJ 1992 bioessays, Rozenschwaig), which is said to have an influence on life expectancy. Ageing and damage of non-dividable cells (such as neurons) appears to be a particular problem for the human organism. Melatonin, as a secreted product of the pineal gland, is more easily absorbed into the cytoplasm of these cells than other antioxidants and could develop a protective effect against radicals. However, the doses necessary for this might possibly be too high and intake would have to begin in childhood and would have unpleasant side effects.

2. Mitochondria theory:

Mitochondria have their own ring-shaped DNA which contains 37 genes. A mutation of mitochondrial DNA (which is only inherited via the mother’s ovum) can lead to a disturbance of the electron transport within the mitochondrial respiratory chain, leading to excess formation of free radicals which damage the mitochondria themselves and the cell as a whole (in particular the cell proteins and receptors). The central nervous system is most dependent on the steady energy production of the mitochondria. There is a theory which says that an age-related decrease in energy production by the mitochondria associated with damaged proteins is significantly involved in the development of age-related degenerative illnesses (Alzheimer’s disease, type II diabetes, dementia…). Furthermore, mitochondria are particularly sensitive to pollutants which affect us for life. The mitochondria are missing histones which make DNA damage more unlikely. 

ENERGY THEORIES:

1. Energy consumption theory:

It is possible that the entire life energy conversion per weight unit of many different species is limited to a certain maximum value. The slow-moving tortoise consumes relatively little energy per gram of body weight (added up over its entire lifetime) and lives for a relatively long time, while the more restless and agile mouse only lives for a short while. To put it more simply; the more an animal eats in relation to its body weight, the shorter a lifespan it has.
Examples:

Mouse: 250 cal/gr = 18 months, Pig 12 cal/gr = 300 months
In this vein, fasting or starving also has an influence on life expectancy. A lifelong hypo calorific diet increases life expectancy in animals, but also in single-cell organisms. It has now been proven to be the case for mice, rats, fish, flies and spiders. Humans who lived to a great age were mostly slim. Hunger keeps these animals young and delays the appearance of typical age-related diseases. The introduction of a low-calorie diet in adulthood still has an effect and can delay the development of cancer until old age.

This theory is probably an aspect of the above-mentioned theory which supposes that cell damage from metabolic products effects the life expectancy of an organism. Observation of apes who are being given a diet with a 30% reduction in calories is currently taking place. In approx. 20 years, it will be discovered whether they have lived for longer than apes who had free access to food. A decrease in total metabolism due to hunger does not appear to be the reason for the extended life span, as an increase in metabolism following cooling increases life expectancy somewhat (J Appl Physiol 1986 (61)).

We also support this theory: a high-calorie diet, sport, stress etc. create large amounts of free radicals. With dietary supplements, so-called radical interceptors, the damaging effects of radicals can be prevented and life can still be enjoyed to the full.

2. Glucose and AGE theory (glycation theory of ageing by Anthony Cerami):

Patients suffering from stress/burnout syndrome have high insulin levels resulting from the low levels of its opposite number; adrenaline. This leads to increased glucose being transported into cells. This, along with other sugars, creates networks due to a non-enzymatic pathway with proteins (e.g. collagen) which impair cell function and promote ageing. This process is called “non-enzymatic glycosylation” and is also the process which alters haemoglobin when at high glucose levels in such a way that past glucose levels can be seen from the concentration of glycosylated haemoglobin. Carbonyl groups in sugar bind to amino groups in proteins. The products formed by this are called “advanced glycation end products”, or AGE for short (Baynes 1991).
In turn, these AGEs bind covalently to other macromolecules and contribute to the age-related damage such as that which often occurs with diabetes. AGEs can also influence cellular receptors (e.g. fat metabolism). AGEs seem to be the reason for the decrease in muscle tissue with advancing age. They also appear to play a role in Alzheimer’s disease and AGE inhibitors have also be successfully tested with Alzheimer patients. AGEs are also linked to the development of cataracts.

3. Thymus theory:

The immune response to infection diminishes with age. At the same time, autoimmune diseases in older people are on the increase. A sign of ageing is the shrinking (involution) of the thymus gland to a retrosternal fat body with age. In very old age there is then a “global failure” of the immune system (Roy Walford, CR supporter).

Human life expectancy through the ages: (from various sources)

  • Prehistoric time: approx. 25 years
  • Greece 550 B.C.: below 20 years
  • Rome at time of Christ: 30 years
  • Germany 1800: approx. 30 years
  • USA 1870: 40 years
  • Germany at the end of the 19th Century: < 40 years
  • Germany 1950: < 70 years
  • USA 1955: 70 years
  • USA 1996: 79 years
  • Estimate for 2050: a little over 80 years

Hypothetical person with a long life expectancy:
A (Caucasian) woman who is either infertile or has been preventatively sterilised, who is a non-smoker and has high levels of uric acid (and possibly gout), who is subjected to low levels of stress as a result of a tendency towards mental and physical inertia, who has been hungry since birth and whose parents also lived to a great age but who were young when she was born. She would like to sleep for at least 8 hours per night during adolescence, take safflower oil, fish oil, eat sensible amounts of vitamin E and garlic, avoid foods which are high in calories and laugh vigorously at least once per day. Her intelligence and income are not particularly high, although she is not poor. She would avoid infections in adulthood by any means necessary, but go through childhood diseases. She would wash and clean her teeth regularly. Her melatonin levels would remain normal in old age. She would rarely leave the house in order to avoid accidents and she would also avoid public roads and long journeys. She would always wear a seatbelt in the car. She would go to church on Sundays (regular church goers have a higher life expectancy). All in all, this appears to be a way of living for longer, although it does not seem to be particularly enjoyable. Here at INAKARB, we would like to help our clients to achieve a long and happy life.

In October 1998, the world’s oldest person seemed to be Sarah Knauss, who reached the age of 118 on 24.09.1998 (http://www.grg.org).
In 1997 Jeanne Calment died in France aged 122 (she still cycled at the age of 100).
In 1986 Shigechiyo Izuma from Japan died aged 120 years and 273 days. Whether Mr. Wanyingi in Africa was actually born in the year 1870 has not been confirmed. If so, he would be the world’s oldest person by far.

Particular illnesses which are to do with premature ageing:

  • Progeria – Hutchinson-Gilford syndrome with premature ageing and with a life expectancy of below 20 years. Occurs once in every 4 million births. Caused by spontaneous mutation. Not inherited (significance of hyaluronic acid?) 
  • Werner syndrome – Progeria in adults. Recessively inherited. Life expectancy below 50 years. 
  • Xeroderma pigmentosum

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