Lupine Publishers | Scholarly Journal of Food and Nutrition
Short Communication
During the last half-century, human
beings have developed new processes to both produce and preserve food for
immediate and long term consumption. Such abilities would presumable result in
increased survival of the species by reducing starvation and provide for times
of need. The exact opposite has occurred; however, with recent increases in
obesity and weight related disease (eg. heart disease, diabetes mellitus,
hypertension, certain forms of cancer, et cetera) leading to an increase in the
incidence of these diseases and related deaths. Arguments over who is to be
blamed for these increased health problems has lead to various discussions
implicating the food industry, the government, the pharmaceutical industry, and
others, with efforts to even blame our ancestors by convincing ourselves that
it is our genetic nature guised in the politically acceptable term, the
“thrifty gene” hypothesis which is to blame. In fact for many people, any
explanation except for individual accountability is an acceptable cause for the
problem, but failure to correct the cause of the problem does not solve the
problem, it merely masks it [1-4].
Having been involved in research
[1-26] for almost four decades involving heart disease and the dietary factors
which produce the inflammatory changes within our bodies which lead to this
immunologic disease, it is clear that we need to consider this problem from a
more fundamental perspective, namely a discussion of nature (that which we are
genetically born with) versus nurture (those behaviors we exhibit in
perpetuation of the species). The changes in our production, storage,
utilization and consumption of food is clearly a change in behavior and such
changes in behavior occur much faster than genetic mutation can occur. As we
are seeing, the wrong behavior in any situation can be threatening to the
survival of the species. Survival of the fittest proposes that only those
species with the genetic predisposition for survival, which also exhibit the
behavioral traits for survival, will endure changes presented to them. These
changes may occur from sources outside the control of the species (eg. volcanic
eruptions, temperature changes, meteorite impaction, et cetera), or they may be
precipitated by the species itself. Like all species, we Homo Sapien Sapiens,
have the ability to affect our environment for better or worse. In our earlier
development, decisions to leave areas of protection (trees, caves, et cetera)
and venture out into open areas where we were exposed, produced a situation
where we were more the hunted than hunter. These efforts were successful, not
because of a sudden genetic shift in the species (there is no data to support
such a theory), but rather, a shift in our behavior (the ability to make and
use tools/weapons) and our working together to out think our more physically
agile and aggressive opponents. Those human ancestors who did not adopt such
behavioral changes, but ventured out onto the plains without the necessary
behavior to ensure their safety, undoubtedly provided lunch for other species
which was the more fit for their environment. Hence, survival of the more adept
species prevailed [5-8].
In the February 7, 2003 issue of
Science, several authors discussed the need to further understand the
neurohumoral pathways involved in the regulation of eating - hunger versus
satiety. While such efforts are of scientific value, our focus as a society
appears to be more related to the pharmaceutical development of drugs to
manipulate these pathways than the understanding that behavioral change is
needed. In other words, the focus has been to influence nature and not nurture.
Such efforts fail to recognize the multiple lessons from the past that we
should have learned regarding our efforts to manipulate nature, ignoring the
impact of nurture, which can lead to serious consequences [9,10]. The issue
here has not been a change in the genome of the human species, but behavioral
changes which threaten our survival. For example, the genetic structure of
Japanese immigrants who have migrated to the United States in the last 50
years, has not been associated with a genetic shift in the population, yet
changes in the consumption of high fat, high calorie foods has lead to an
increase in heart disease, diabetes mellitus, obesity, elevated lipid
(cholesterol, triglycerides) levels, and certain types of cancers, when
compared with their Japanese ancestors of only two generations earlier. Similar
problems have occurred among the children of China and Spain in a single
generation; reflecting changes in (behavioral) eating patterns and not genetic
shifts. Other groups frequently discussed, to support the need for manipulation
of the neurohumoral pathways include the PIMA Indians, who have demonstrated a
significant increase in obesity and diabetes during the last several decades
resulting from changes in dietary and lifestyle habits, which when coupled with
their leptin resistance, accelerated their inherent risk of disease; however,
their leptin resistance existed long before their dietary changes and did not
produce a health problem until changes in dietary patterns occurred following
high calorie, high saturated fatty foods provided by the US government. Hence,
the presence of a potential genetic problem was not realized until the
behavioral changes occurred to make the problem a reality [11-18].
Efforts to manipulate the chemical
processes of our bodies may result in more devastating problems than we
currently have or are presently capable of understanding. For example, numerous
anorexic medications have been used in an effort to result in weight loss.
These medications have resulted in ocular problems [27], pulmonary problems
[28, 29], hepatic [30] problems, and valvular problems [31-35]. Leptin itself
was discussed throughout the Science articles as a regulator of hunger and like
so many other substances found in the human body; leptin has more than one
effect. It is now known, that leptin is involved with immunologic response and
altering leptin levels whether by medication or dietary efforts, may improve
heart disease by reducing the inflammatory component of the disease [19,20].
The utilization of medications may however affect more than just this component
of leptin while the dietary changes which reduce caloric and saturated fat
content have been shown to lower weight, which will not only reduce leptin
levels, but the other inflammatory components of heart and other diseases as
well. Our studies [2-14, 18, 20-21, 23-26] have looked at both the behavioral
component of changing eating habits as well as the effect of medications. These
studies have clearly shown that the successful approach to weight loss must
include several key components. The problem is a behavior of excess consumption
of calories and fat, not an excess of food availability. Individuals must make
decisions several times a day regarding food consumption and the type of food
they will consume. They do so based upon the information they hear and read.
Clever advertisements and marketing by people hoping to profit by influencing
human behavior has lead to more misinformation than information. These
strategies have been used previously by suppliers of tobacco and alcohol
products and clearly focus on influencing behavior and not genes [21-25].
Our research [2-14, 18, 20-21,
23-26] has shown that people clearly can loose weight and keep it off, by
changing their eating behaviors. To do this one has to first accept that this
is a behavior problem, which can and must be influenced through changes in
behavior alone, instead of resigning to a naïve assumption that our genes are
driving us to over consume food. An interesting twist on this approach has been
the popularization of diets, which tell people they can consume as much food as
they want and still lose weight. These extreme diets may suggest that one
component of the diet alone is at fault, negating almost a century of
scientific work establishing the need for balance with reduction in total
caloric and saturated fat intake [26,27]. In fact, the reason for the success
of such extreme diets is the reduction in total caloric intake, which results
in weight loss. The second law of thermodynamics still applies! The consequence
of extreme diets, however, is the potential adverse effects seen when heart
disease, kidney disease, liver disease, bone disease and other health problems
occur. As our research has shown, changes in eating behaviors with a balance in
protein, carbohydrates and fat is not dependent upon the gene pool of people
changing their eating patterns. Many eating patterns are learned (home, school,
work, et cetera) and can be influenced through these same groups [29-32].
In the mid 1900s, we as a species,
for better or worse, learned how to increase our production of our food, as
well as our preservation of food by hydrogenation. We have not focused nearly
enough on the quality of this food and its impact on our health. In 1999, as a
member of the University of Northern Iowa advisory board, I was asked what I
thought the greatest healthcare problem would be for the United States in the
next century. My response, then as now, was simple and concise. Unless we
change our current eating behavior we will become a bimodal society. My
explanation is as follows. Those members of our society who have taken better
care of themselves have not only benefited from this health of earlier years,
but can currently take advantage of our ability to keep people alive longer.
While we can extend the quantity of life, this does not mean we are improving
the quality of life. Our school age children (those from Kindergarten through
12th grade) are showing ever-increasing problems resulting from increased
weight and sedentary lifestyles. These problems affect ¼ to 1/3 of these
children and include heart disease with elevated cholesterol levels, high blood
pressure, diabetes mellitus and problems with weight (both overweigh and
obesity). This increased incidence of health problems could very easily result
in our children dying in their 20’s-50’s instead of their 70’s-80’s. As a
consequence, the average life span will decrease. They will live long enough to
conceive. This will, in the short span, lead to a stable population of children,
and a stable population of older adults with a drop in numbers of people
between 30-60 years of age. This bimodal population will lead to a healthcare
crisis for two major reasons. First, the increased cost of caring for
increasing numbers of people with heart disease, diabetes mellitus,
hypertension, and certain types of cancer, and secondly, because the adults who
will be responsible for paying the taxes (30-60 year olds) to pay for
healthcare will be fewer in number. This reduction in individuals financially
supporting the healthcare system will result in a financial burden that cannot
be maintained and the system will collapse, resulting in problems with delivery
of healthcare and further problems. Perhaps this is the crisis, which will be
necessary for us to change our behavior, analogous to watching our ancestors
being eating on the Serengeti [33].
However, unlike natural disasters,
which we cannot directly influence, we have produced this one and the human
species need not eat itself into extinction. The same efforts being employed to
develop drugs to manipulate our genetic response to eating could be put to
better use to produce foods which have higher nutritional values, with less
saturated fat and more complex carbohydrates. These foods are produced by many
of the same companies who make the medications we take as a society. Similarly,
our efforts could be directed towards improving our dietary and exercise
patterns, beginning with our children and incorporating all age ranges. This
would be considerably less costly to our society than the scenario outlined
above. Like our eating behaviors, the decision to change the foods we make
available for consumption, is also a conscious (behavior) decision, which in
the end may determine the survival of the species. The only question is have we
evolved enough to survive or just enough to cause our own extinction [34-36].
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