"Nothing from nothing leaves nothing..."

Copyright 2007, James Michael Howard, Fayetteville, Arkansas, U.S.A.
(...that is unless someone else has already said this ...I tried to find this on the internet and could not find anyone else has... I will remove this copyright if I do.)

This thought has occurred to me lately, after thinking about it for a few years. What if the "nothingness" of the universe still exists? I think that the nothingness is still here; nothing has simply changed form. I suggest the "universe" is simply a conglomeration of positive and negative material that, if combined properly, would simply result in nothing.

That is, nothing has changed. The nothingness still exists, only in a different form. Therefore, gravity would be the attraction that tries to reunite the separation of nothing into two forms. The "Big Bang" is simply the change of nothingness to a different form.

Gravity and black holes are simply the mechanism of return to the condition of the "universe" before the big bang.

The "Obesity Epidemic in Children" and the World

Testosterone reduces leptin. Leptin reduces appetite. Therefore, children of higher testosterone have less appetite suppression. It is my hypothesis that the percentage of individuals of higher testosterone is increasing. Therefore, overeating is increasing. This may account for the obesity "epidemic" in the U.S. (Additionally, testosterone stimulates ghrelin which stimulates appetite; see second citation, below.) (Copyright 2003, James Michael Howard, Fayetteville, Arkansas, U.S.A.)

"Relation of race, age, and sex hormone differences to serum leptin concentrations in children and adolescents.

We explored the effects of race, age, and sex hormones on the serum leptin concentrations in 203 white and 88 black children and adolescents (ages 9.3-20.5 years). A significant sex by race interaction on serum leptin levels (p = 0.0301) was observed with lower serum leptin concentrations, adjusted for subscapular thickness and age, in black boys than in white boys. Girls had serum leptin levels that were on average 2.15 times those of boys (p < 0.0001). There was an age by sex interaction (p < 0.0001) with serum leptin concentrations decreasing in boys but not in girls with age. A strongly inverse relationship of serum testosterone levels with serum leptin levels in boys (p = 0.0067) appeared to explain this effect of age. In conclusion, the serum leptin concentration is slightly lower in black boys. A higher testosterone level in boys appears to account for an age-related decline in serum leptin in boys and the overall lower levels in boys than in girls." (Horm Res. 1998;49(5):240-6)

"Testosterone replacement therapy restores normal ghrelin in hypogonadal men.

We recently described a connection between androgens and ghrelin in women affected by the polycystic ovary syndrome. To further investigate the interaction between sex steroids and ghrelin, we investigated circulating ghrelin levels in a group of hypogonadal men before and after therapeutic intervention aiming at normalization low testosterone (T) concentrations. Seven hypogonadal men were compared with nine overweight/moderately obese men matched for body mass index and body fat distribution parameters, as well as with 10 normal weight controls. Total and free T and plasma ghrelin levels were significantly lower in the hypogonadal men than in the control groups. Hypogonadal men also had a significantly higher insulin resistance state. Ghrelin levels were positively correlated with both total and free T concentrations. A significant correlation was also found between ghrelin and the anthropometric parameters and the insulin resistance indexes. However, in a multiple regression analysis in which a correction for all covariants was performed, only the relationship with total and free T persisted. After the 6-month replacement T therapy, ghrelin levels of hypogonadal patients increased and did not differ significantly in comparison with both control groups. The positive correlation between ghrelin and androgens still persisted after T replacement therapy, after adjusting for confounding variables. These data further indicate that sex hormones modulate circulating ghrelin concentrations in humans. This may be consistent with the concept that ghrelin may exert a relevant role in the endocrine network connecting the control of the reproductive system with the regulation of energy balance." ( Clin Endocrinol Metab. 2003 Sep;88(9):4139-43)

It is my hypothesis that human evolution is directly influenced by testosterone levels and this appears to be supported (see human evolution ). The mechanism is differential reproduction within the population. That is, individuals of higher testosterone will have a reproductive advantage over those of lower testosterone. Individuals of higher testosterone will be more aggressive and exhibit increased libido; over time they will reproduce faster. I suggest this is ongoing and identifiable today as the secular trend , the increase in size and earlier onset of puberty. The secular trend is considered by some to result from increased nutrition. I suggest the secular trend is simply accelerated by increased nutrition. Reproduction is simply increased by better nutrition. This is the "feed and breed" phenomenon.

Over time, the percentage of individuals of higher testosterone will increase. As testosterone increased within the hominid line, beneficial effects accrued. Hence, human evolution is progressive. However, it is part of my explanation of human evolution that periodically testosterone levels are produced that are harmful to our species. Hence, human evolution exhibits periodic extinctions of certain hominid groups. At these times groups of lower testosterone survived. However, following extinction, or population decelerating, events, the increase in individuals of higher testosterone automatically resumes. Individuals of high testosterone exhibit characteristics that are considered negative. I suggest this is currently being expressed within human populations. The percentage of higher testosterone individuals is increasing and so are their characteristics. One example is the increase in female breast cancer, which I connected with increased testosterone in 1994 (see " An Explanation of Cancer and the Increase in Cancer .") In 2002 this was supported: "...testosterone might be more strongly associated with [breast cancer] risk than estradiol." Journal of the National Cancer Institute 2002; 94 : 606-616. My point is that the percentage of individuals of higher testosterone may periodically increase and this may be identified within current populations and populations of the past. I invite you to read any of the articles below that may interest you.