• The Delayed Disease Bomb

    Posted November 7, 2018: by Bill Sardi

    A biological reality is that many Americans may have been genetically pre-programmed to develop diabetes, heart disease, high blood pressure, become obese, even suffer with mental depression and other mental problems, based upon circumstances in their mother’s womb and very early childhood.  That is when the human library of ~25,000 genes that resides in the nucleus of every living cell in the body develops what are called epigenetic tags or marks.

    Genetics is the arrangement of steps (nucleotides) on the DNA ladder that is fixed whereas epigenetics involves the dynamic protein-making aspect of genes (called gene expression or gene silencing) that helps humans adapt to their immediate environment.

    Repeated exposure to a nutrient or chemical prior to birth or during early childhood development can result in an epigenetic mark or tag that is heritable even to subsequent generations.

    DNA: genetics vs mutation vs epigenetics vs

    Childhood growth may mask these epigenetic propensities and these characteristics may not materialize till later in life.  Or even more disconcerting, the epigenetic programming of our great grandparents may be passed on to succeeding generations and influence their great grandchildren today.

    These long-term effects are now referred to as Developmental Origins of Health & Disease.

    Human genes are programmed in the womb and early childhood development.  Epigenetic marks are made to produce a proclivity towards health or disease that may occur immediately or not emanate till later in life.  The trigger for this delayed epigenetic response may be inflammation or iron overload.

    Molecular reprogramming of our genes

    Humans are genetically programmed from the womb and infancy based upon their mother’s nutrient status that can lead to obesity and leptin resistance.  Leptin is the hormone that signals when to stop eating (the satiation factor).   These early developmental time windows, when genes can be molded, are critically important. For example, there is programming in the hypothalamus in the brain to sets our appetite for life.   How much we eat may be epigentically pre-determined by leptin, a hormone that controls satiation and appetite.

    When the brain cannot register enough food has been consumed due to leptin resistance there is susceptibility to overeating and obesity.  When leptin is not recognized in the brain (leptin resistance) then more and more food is consumed producing even greater amounts

    Breast-fed infants have higher serum leptin levels compared to formula-fed infants, which increases the risk of being obese.  Likewise, during pregnancy there is natural leptin resistance to ensure the mother consumes enough food for a growing onboard fetus.  High estrogen levels combined with leptin resistance after birth can signal mothers to keep eating volumes of food and after birth mothers can become as wide as the front door if they don’t exercise to curb estrogen dominance (exercise promotes testosterone).   Their future babies will be prone to develop metabolic problems.

    Over use of antibiotics

    Young infants exposed to antibiotics are also more likely to become obese later in life.  Even prenatal use of antibiotics appears to induce obesity in children. Antibiotics are given to cattle to fatten them for slaughter.  Antibiotics may quell infectious threats to life in young infants but expose them to obesity, allergies and behavioral problems.


    Cesarean section delivery of newborns is on the increase.  The number of births by C-section worldwide nearly doubled during the period 2000 to 2015.  Natural childbirth colonizes the newborn’s gut with bacteria transferred from the mother, which is a crucial factor in the newborn’s immune system.  C-sections avert this mother-to-newborn transfer of healthy bacteria to the child’s gut.  Cesarean sections are associated with increased risk for obesity is school childrenChanges in gut bacteria reprogram the bacterial genes.

    Fructose reprogramming

    When the field of Developmental Origins Of Health & Disease was in its infancy in the early 1980s, scientists witnessed an unprecedented increase in adult-onset diabetes from 108 million in 1980 to 422 million in 2014.  The food industry, by virtue of its introduction of high fructose corn syrup that is now found in peanut butter, meats, cereals, ice cream and other processed foods, re-programmed the brain to overeat.  The objective of the food industry has been to get consumers to eat a box of cookies to the bottom.  Brain pleasing foods are engineered and consumers are then blamed for eating them and losing control of their appetite.

    High-fructose maternal diets in the womb predispose offspring to develop high blood pressure, particularly in males, later in life.   Of even greater concern is that maternal high-fructose diets impair thinking in the hippocampus of the brain due to altered gene expression.

    Bisphenol A reprogramming

    The explosive increase of Type I child onset diabetes goes unexplained.  Exposure to hormone disruptive chemicals is suspected because of their widespread use.  Pregnant women are exposed to numerous hormone disruptive chemicals that can cross the placenta and enter into the fetus to produce lifelong adverse effects.  The beta cells in the pancreas that produce insulin are affected.  Adverse changes may occur prior to birth or in early childhood.  Bisphenol A is one such hormone-altering chemical.

    To add to the problem, modern humans are now exposed to various hormone- altering chemicals like bisphenol-A (BPA) and phthalate plasticizers that are associated with abnormal insulin secretion and inability to utilize insulin (insulin resistance).  Even when exposed to low doses of BPA in the microgram per body weight per day hormonal effects were recorded in the brain of lab animals.

    Normally toxicity studies are done prior to use of chemicals.  But in this instance the need for toxicity studies may not have been apparent because of latent effects even generations distant from the original exposure.  Now a horror story is unfolding.  The field of population epigenetics is just now emerging, decades late.

    Nearly 90% of the U.S. population has traces of bisphenol A (BPA) in their urine.  Primary exposure comes from plastic bottles or packaging.  Brain structure is affected by BPA.

    Exposure to bisphenol A in laboratory mice leads to a unique genetic signature that is associated with behavioral changes.  BPA exposure during pregnancy has been shown to alter genes in the hypothalamus of the brain of laboratory animals.

    The diethylstilbesterol (DES) disaster is well known.   DES, a synthetic estrogen, was prescribed to pregnant women between 1940 and 1971 to prevent miscarriage and premature labor.  DES was not only proven to be ineffective in preventing these problems but was linked to cancer of the cervical and vaginal tissues later in life.  DES babies have 40 times greater risk for development of lower genital tract cancer than unexposed women.  But a more recent source of similar concern, bisphenol A, a plasticizer, is well documented but next to nothing is done to inhibit exposure.  BPA is now in the water supply and foods and beverages.  BPA is used in inks on cash register receipts where it is unwittingly transferred from fingers to skin and absorbed.  BPA is present in 95% of the population over 6 years of age.

    Developmental exposure to BPA increases susceptibility to breast cancer.  Experts now say BPA should be considered a direct mammary gland carcinogen.  The FDA Response to this gender-bending BPA chemical has been meek.   The FDA now prohibits BPA from baby bottles and sippy cups.  Meanwhile, phthalates have now been shown to feminize boys by knocking testosterone out in their brains.

    The branching of blood vessels in mammary glands of BPA exposed tissues is shown below.

    Comparison: staining in kidney tissues

    Difference between normal (left) and bisphenol A-exposed (right) breast tissue.

    Shown in the epithelial tree where most cancers originate.

    Bisphenol A has also been shown to experimentally produce autism in lab animals.


    The delayed symptomology of early exposure to gene-altering chemicals is observed in zebra fish.  PCBs, or polychlorinated biphenyls, are used in industrial applications and were banned in the U.S. in 1979.  PCBs are highly toxic suspected of causing birth defects.  It has been shown in zebra fish that early developmental exposure to a PCB exposure did not affect embryos but did, via genetic reprogramming, alter normal development and result in adult behavioral changes.


    Low birth weight is a common predictor of health problems later in life.  In an effort to help these infants survive they may be exposed to chemicals such as the anesthetic ketamine during surgical procedures.  A single exposure to ketamine in animals results in mental performance deficits later in life.   More and more infants that are born prematurely and of low birth weight and now survive.  There is a growing concern these premies will lead to an explosive increase in health and mental problems in their adult years.

    Low birth weight may give rise to osteoporosis, spontaneous hypothyroidism, mental problems like schizophrenia and depression later in life.  Low birth weight is associated with mental depression as measured at the 68th year of life while large head circumference and tall height protect from mental impairments late in life.

    Horror story that won’t go away

    This is an ongoing horror story that won’t go away.  And the story gets worse:

    An explosion in adult kidney disease is now realized to have emanated from developmental programming prior to birth and in early development.  Researchers are exploring reprogramming as therapy.

    Prenatal mental depression in the mother is predictive of mental depression in offspring up to 25 years following birth.  Maternal prenatal mental depression is associated with known markers of inflammation (C-reactive protein).

    Normally geno-toxins would be tested before entering human environments.  But in this instance these genetic toxins, which are ubiquitous, are already in play.  Efforts to restrict or ban these agents and practices appear to be too little, too late.

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