Chapter 19: How to Live Longer

 

Let me start by re-stating that the subjects of these chapters are interrelated, which make it difficult to construct a logical story. This is to be expected because the Mathematic of the Mind is all about moving between logic points or attractors. So, consider the last paragraph of the previous chapter.

 

But during life, there is a change in intelligence, as indicated above, and a multitude of papers have been written which compare the intelligence of races. Of course there are different levels of IQ in the different races, but they have occurred because of upbringing, poor food, lack of stimulation, infections, poor parenting, arguments in the household etc. Not only is intelligence reduced, but mental health in the child may be impaired under these conditions.

 

Firstly, ‘during life, there is a change in intelligence’. As stated before, we come into life in the simplest state so that we can start learning using all of our faculties and senses. I believe that child prodigies are ‘taking over’ the frantic learning ability that is designed to ‘fast track’ us into the new (out of womb) world where the slow to learn end up as something’s lunch. There can be psychological or personality problems, later in life if the child is ‘pushed’ too hard to perform.

 

Most of the hard work is done within the career path, which lasts for decades. Consider the quotation from Mozart, previously, where the child prodigy tells how it took him decades of hard work to become a composer of worth. Successful hardworking people need years of work to build a life for their family. From an aging point of view, the members of the race will eventually have a longer length of life if the male, that is used, is very old, yet hale and healthy. This is at odds with nature’s way, which uses males in the prime of life. Also, it has been shown elsewhere that sperm from older males is perfectly good to use, and in the chapter on super-eusociety, there is an efficient means to increase people’s length of life in this way.

 

The maximum present life span for humans is currently about 120 years. We all know that fewer people reach the more advanced age of 100 plus and occasionally we hear that the oldest person has died, near the 120 year level. Thus, the best that we can hope for, and aim for, is to remain active and healthy to 120 years of age, and then die. But, is this really true? It has been argued previously that many of our major organs can be classed as components. Why can’t we view the human body as a component of a group? After all, it appears that exercising the brain increases IQ and increasing exercise increases strength and power in our muscles, so, can we increase our current life span? So, if the body is a component and will accommodate any reasonable need, what can we derive about length of life? Looking at this question in the simplest form, we can say, that treated ‘well’ or even ‘very well’, that the body may last to a maximum of 120 years. But, what if we change our lifestyle significantly, has the body got the capacity to live longer in certain circumstances?

 

‘Among mammals, there is a good general relationship between size, metabolic rate, and longevity. Across the size range from mice to elephants, the smaller creatures generally live faster – having a higher metabolism but a shorter life span, leading to the popular perception that a species is allotted only so many heartbeats. With deepwater fishes, however, this is not the case. The meso- and bathypelagic fishes, despite their greatly reduced metabolism, generally live less than 10 years, much the same as an active pelagic species of similar size; for example an anchovy or pilchard. Benthopelagic fishes living over the continental slope, such as the macrourids (Coryphaenoides spp.) or sablefish, have a greatly reduced metabolism but also generally live for around 50-75 years – which is much longer than comparable species on the continental shelf, such as the Atlantic cod, which lives to about 25 years. At the far end of this continuum , several of the key species living on seamounts, such as the orange roughy and oreos, though growing to only about 50 centimertre, can live for an extraordinary 100-150 years.’ (The Silent Deep, Tony Koslow, p 130)

 

It does not matter to us, at the moment, why these fish live for so long, especially considering their size, it is the fact that they can! Fish are not that different to us in basic form, as was shown, previously, they have the same basic brain structure (for a start). Continuing, ‘Opportunities for young fishes to successfully recruit into this environment may be as limited as chances for young trees to grow up beneath a mature forest canopy. Little wonder, then, that orange roughy do not recruit to the seamount until they are adults, about 30 centimetres in length and 25-30 years of age, and that their reproductive life then extends for the next 100 years or so. As noted earlier, competition is so severe among the adults that they may build up the requisite energy reserves to spawn only every other year.’ (p 132)

 

Interesting, but what does it mean? I have previously mentioned that the usual interpretation of ‘survival of the fittest’ require a niche or closed environment. The seamounts are just such an environment, which is isolated and supports only a few predators. ‘There is strong circumstantial evidence that orange roughy have co-evolved with large predators and have developed striking, albeit still poorly understood sensory systems and behavioral adaptions to avoid them.’ (p 131) What this is saying is that fish (at least) have the capacity to live a long lifetime when necessary and the trigger appears to be that the competition among themselves reduces the food supply which reduces the breeding. This does appear to be in line with the body being a component as there is negative feedback (less breeding) in times of over-population.

 

The important point of the above is that it suggests that a long lifetime is available, under certain circumstances. Is this effect general across the species? It would appear so, but from our point of view, experiments on rats would be more compelling. So, ‘A life‑span study was carried out on longevity, pathologic lesions, growth, lean body mass and selected aspects of muscle of barrier‑maintained SPF Fischer 344 rats fed either ad libitum (Group A) or 60% of the ad libitum intake (Group R). Food restriction was as effective in prolonging the life of already long‑lived SPF rats as previously shown for rats maintained in conventional facilities. Food restriction not only increased the mean length of life but also acted to extend life span since more than 60% of the Group R rats lived longer than the longest lived Group A rat. Renal lesions occurred at an earlier age in Group A rats than in Group R rats and progressed more rapidly. Death of most Group A rats was associated with severe renal lesions while few Group R rats showed such lesions at death. Food restriction was also found to delay or prevent interstitial cell tumors of the testes, bile duct hyperplasia, myocardial fibrosis and myocardial degeneration. Gastrocnemius muscle mass declined in advanced age and food restriction delayed this decline. Interestingly, however, lean body mass did not progressively decline with increasing age but rather decline occurred only after the onset of the terminal disease process.’ (Life span study of SPF Fischer 344 male rats fed ad libitum or restricted diets: longevity, growth, lean body mass and disease, J Gerontol. 1982 Mar;37(2):130‑41., Yu BP, Masoro EJ, Murata I, Bertrand HA, Lynd FT., Abstract)

 

So, to simplify, food restriction not only increased the mean length of life but also acted to extend life span, Renal lesions occurred at an earlier age in Group A rats than in Group R rats and progressed more rapidly, Food restriction was also found to delay or prevent interstitial cell tumors, and interestingly, however, lean body mass did not progressively decline with increasing age but rather decline occurred only after the onset of the terminal disease process. So, it appears that rats that eat less live longer, they are healthier with less tumors etc. and interestingly (their word) body mass did not decline with age.

 

However, it should be noted that the effect for the rats is different to that of the orange roughy. The orange roughy are eating a diet that they have evolved with, albeit in short supply, but the rats are being fed a ‘man-made’ restricted diet. The longer lives of the restricted rats could have occurred because the food is not what they should be eating, but was all that they had to eat.

 

It is possible that rats have this same mechanism for increasing their life span and healthiness as the orange roughy etc. But, people do not like to restrict their food intake to the point of hunger, so we have to find a way around this problem. Another study, ‘previous investigations suggest that increased life span of calorie‑restricted rodents is a function of caloric intake rather than the macro‑ or micronutrient composition of the diet. However, the dietary source of carbohydrate has not been widely investigated. We hypothesized that the dietary carbohydrate source may affect the life span of rats independent of caloric restriction. This hypothesis was tested in male Fischer 344 rats fed ad libitum or restricted to 60% of ad libitum, an isocaloric diet containing 14% protein, 10% fat, and 66% sucrose or cornstarch. Body weights of the ad libitum‑ and restricted‑fed sucrose rats were consistently greater throughout the experimental period compared to diet‑matched animals. Food intake did not differ significantly. The survival curves of ad libitum starch‑ vs sucrose‑fed rats were significantly different. That is, the mean, median and upper 10th percentile survival were significantly greater in the ad libitum starch‑ vs sucrose‑fed rats (mean life span: cornstarch‑fed, 720 +/‑ 23 days; sucrose‑fed, 659 +/‑ 19 days). Calorie‑restricted starch‑fed rats had poorer early life survival, and no significant increase in mean life span compared to ad libitum cornstarch‑fed animals (726 vs 720 days). These animals did, however, have the greatest upper 10th percentile survival of all four experimental groups. Mean life span of calorie‑restricted sucrose‑fed rats was significantly greater than that of all other groups (890 +/‑ 18 days). The differences in survival rates between sucrose‑ and cornstarch‑fed animals could not be attributed to the effects of carbohydrate source on body weight, energy absorption, or on the timing and severity of the pathological lesions normally associated with aging and/or caloric restriction in this species. These data support the hypothesis that the dietary source of carbohydrate, i.e., sucrose vs cornstarch, can significantly affect life span independently of caloric intake.’ (Source of dietary carbohydrate affects life span of Fischer 344 rats independent of caloric restriction., J Gerontol A Biol Sci Med Sci. 1995 May;50(3):B148‑54., Murtagh‑Mark CM, Reiser KM, Harris R Jr, McDonald RB., Abstract)

 

To simplify, the survival curves of ad libitum starch‑ vs sucrose‑fed rats were significantly different. That is, the mean, median and upper 10th percentile survival were significantly greater in the ad libitum starch‑ vs sucrose‑fed rats (mean life span: cornstarch‑fed, 720 +/‑ 23 days; sucrose‑fed, 659 +/‑ 19 days). Also, calorie‑restricted starch‑fed rats had poorer early life survival, and no significant increase in mean life span compared to ad libitum cornstarch‑fed animals (726 vs 720 days). Finally, mean life span of calorie‑restricted sucrose‑fed rats was significantly greater than that of all other groups (890 +/‑ 18 days).

 

Interesting! To simplify further, ad libitum starch is better than ad libitum sugar, it makes no difference with ad libitum starch or restricted starch, and a limited amount of sugar is necessary for a long life. However, the same objection must be raised here as was raised above that a rat is a sophisticated animal that is not properly fed on sugar and corn starch, so there may be other factors that should be taken into account.

 

And simplifying yet again, from the first experiment, we can restrict the nutrients, that is, we restrict the protein, fats and carbohydrates but not the antioxidants, vitamins and phytochemicals by increasing the fibre in the food by increasing use of low-starch vegetables and that added bulk of the low carbohydrate vegetables keeps the body from being perpetually hungry. A recipe that fits this suggestion for an evening meal is a vegetable bolonaise (with cheese, olive oil and tomato on top) with vegetables replacing the pasta.

 

From the second experiment, use a little sugar, but mainly fruit sugar because it is more complex, and use a maximum of low starch food, as well as a certain amount of protein and fat. The answer to this problem is nuts and seeds because they contain protein, oil and starch prepackaged into a convenient storable form that is already dried. So, a recipe for the morning might be a mueslie made from a range of seeds, dried fruits and nuts with (skim) milk to moisten and topped with extra fruit such as blueberries, raspberries and prunes (dried plums). It is important to note that only two meals a day are needed, with no snacks! Also, again, ‘interestingly, however, lean body mass did not progressively decline with increasing age’ and this I can confirm! My weight has decreased (and stabilized) until I was within the recommended Body Mass Index, with no restraint on eating or energy!

 

Of course I have cheated in suggesting these recipes because things are not as simple as outlined here, and because I am using knowledge that will be discussed in later chapters. But it is surprising that it is so easy to ‘trick’ the body into moving into certain ‘survival’ modes by replacing lack of food by fibrous foods, which begs the question, what should we be eating? Perhaps we should turn the logic around and say that if we eat less of the ‘prepared’ or manufactured food we will extend our lives, which could be what the experiment is saying!. If we add fibre to the rations so that we don’t go hungry, we live longer, and with a leap of faith, if we eat natural fresh food with plenty of fibre we should live even longer! It is hardly surprising to surmise that if we ate as they did in the Paleolithic, which matches our genes, we could (help) maximize our life span. It is interesting that it is generally acknowledged that the height of people in the Neolithic (farming) communities was about 4 inches lower than the hunter/gatherers of the Paleolithic due presumably to diet.

 

So, from the above, the human body can be considered to be a component of a group, and can change strength, IQ, longevity and much more, such as personality, obesity, cancer, heart problems, stroke etc if the body is handled correctly. Note that some of these medical problems are mentioned in one of the experiments, above. Whilst super-eusociality works for the race, nations, groups and families, the individual must strive to remain ‘at the top of the heap’, otherwise his genes will be lost to later generations.