Genetic Diseases Do NOT exist

Our genes do not contribute to or cause disease outside of the mendelian family. I am not refuting the theory that genes code proteins, and that this is the means in which our genes manifest. But the ideology that our genes have a huge influence over the outcomes of our lives is nonsense. The modern scientist’s creed is that there is a complex interaction between our genes and environmental factors, but ultimately our genes are the more important of the two. This is showcased by our obsession in trying to find genes associated with diseases, traits, mental phenomenon, etc.

Traits

The reality is that there are certain phenotypic traits that are well explained by parental influence. Things like skin, eye, and hair colour are all determined by our ‘genes’. Two Caucasian parents will not throw an Asian baby if they live in Asia. Parental influence plays a huge role, as we will explore in our discussion surrounding Dr. Prices work. That being said, our skin and hair colour can change based on environmental factors such as exposure to the sun. Our eyes also tend to become lighter as we detox our bodies. Look into iridology for more on this topic.

Height

It is believed that DNA accounts for 80% of the influence on human height. Scientists have also identified 700 genes that influence our height. But is this truly the case? We know that toxicity stunts growth. We know that malnutrition stunts growth. Hormone disruptors stunt growth. Air pollution stunts growth. Childhood illnesses (caused by toxicity and deficiencies, germs do not cause disease) stunt growth. It all boils down to toxicities and deficiencies. It certainly seems to be the case that our environment depicts our growth! On this topic, try to think about how an experiment might show such a phenomenon. Specifically, how could an experiment show that an individuals genetic potential was a certain height? How could this be controlled?

Physique

Another example is our physique. Of course, we might not be able to change where our tendons connect to our bones, shaping the foundation of our physique, but we can certainly grow muscle, tighten our tendons by strengthening them, become leaner, become fuller, etc. This is largely determined on how you train and what you consume. Powerlifters train much differently than body builders. And someone training their natural movement patterns trains very different than them both. Each body composition is going to look different to suit the function. Function is determined by training (or lifestyle) which is influenced by subjective goals. 

There are certainly traits that are inherited, that cannot be changed completely environmentally. However, can we induce that diseases work in the same manner? Should we treat diseases as we treat traits?

Dr. Weston A. Price

Facial development is another example that showcases the importance of our environment. Weston A. Price was a dentist and nutrition researcher who, in the early 20th century, studied traditional diets and their impact on dental health and general well-being. His work focused on the diets of isolated, non-industrialized populations, which he believed offered insight into optimal human nutrition. Price’s main observation was that these populations, which consumed diets rich in whole, unprocessed foods, tended to have excellent dental health and overall physical health, with very few cases of tooth decay, dental deformities, chronic illnesses, or even “communicable” illness. He also noted that when these groups adopted modern, processed foods, their health deteriorated significantly, leading to more dental issues, degenerative diseases and high incidence of “communicable” illness.

Price’s research emphasized the consumption of nutrient-dense foods, such as raw dairy, organ meats, seafood, and fermented foods, which were common in traditional diets. Price also conducted experiments with patients, supplementing their diets with these nutrient-rich foods and documenting significant improvements in their dental health and resistance to disease.

Heritability

Notably are Prices observations surrounding heredity. Price emphasized that nutritional factors during prenatal development and childhood were crucial in determining whether genetic potential was fully realized. In his view, when parents followed nutrient-dense traditional diets, their children were more likely to develop strong bodies, good teeth, and overall vitality. Conversely, he argued that when modern, processed foods entered the diet, dental deformities, narrow faces, and susceptibility to disease became more prevalent over successive generations.

He directly observed parents who ate a nutrient poor diet have children with facial deformities. However, if the children, who had dental deformities, returned to the native diet and way of life, their children would have fine facial development. So, toxicity and deficiencies can certainly be ‘passed down’ it is not due to genetic factors whatsoever. This points to the idea that genetic diseases do not exist.

Mendelian Disorders

Gregor Mendel’s study of heredity, conducted in the mid-19th century, laid the foundation for modern genetics. But we could induce many theories from his empirical observations. Mendel, an Austrian monk, experimented with pea plants to understand how traits were passed from one generation to the next. He focused on specific traits like seed shape, flower color, and plant height, choosing pea plants because they had easily observable characteristics and could be bred in controlled ways. By crossbreeding plants with different traits and analyzing the resulting offspring, Mendel observed predictable patterns in the inheritance of traits, introducing the concepts of dominant and recessive alleles.

Types of Mendelian Disorders

There are many types of Mendelian disorders. First, we have autosomal dominant disorders. In these disorders, only one copy of the mutated gene (inherited from one parent) is sufficient to cause the condition. Theoretically, affected individuals have a 50% chance of passing the disorder to each offspring. Examples include Huntington’s Disease and achondroplasia, which is the most common form of dwarfism. Let us return to this in a moment.

We also have autosomal recessive disorders. In these cases, an individual must inherit two copies of the mutated gene (one from each parent) to express the disorder. If both parents are carriers, there is a 25% chance with each pregnancy that their child will be affected. Examples include Cystic Fibrosis, Sickle Cell Anemia and Phenylketonuria.

Lastly, we have the class of X-Linked Disorders. These disorders are caused by mutations in genes located on the X chromosome. They often exhibit different inheritance patterns in males and females, as males have only one X chromosome while females have two. Examples include Duchenne Muscular Dystrophy and Hemophilia.

Dwarfism

Each of the examples could be discussed further, but let us expand on a few to highlight a few observations about the nature of Mendelian disorders. Achondroplasia, or dwarfism, is not caused primarily through heredity.

Around 80% of individuals with achondroplasia have parents with average stature and have achondroplasia as the result of a de novo pathogenic variant. Such parents have a very low risk of having another child with achondroplasia.

Retrieved from this article.

From this we understand that the overwhelming majority of cases are created de novo.

Cystic Fibrosis

Another example is cystic fibrosis. Cystic fibrosis is said to be caused by mutations in the CFTR gene, leading to defective or absent CFTR protein, which disrupts salt and water balance in cells, especially in the lungs and digestive system. There are over 2000 mutations of the CFTR gene that can ’cause’ CF. We are finding new mutations all the time, because we have made our minds up that CF is caused by mutations in the CFTR protein, a beautiful example of theory ladenness. Here we can see that CF might not be genetic at all, but by a trick of the genetic trade their theories are ‘proven’.

Let us work this out. Those that display the the symptoms of CF are subject to genetic analysis, in which variants are found. These variants are complied into a big list of potential mutations that can cause CF. If someone has CF, but their genes do not match the 2000 mutations, this new mutation (which can be a single nucleotide) will be added to the list of mutations to make 2001 mutations that can cause CF. The list will be never ending, and let us keep in mind that the CFTR mutation was discovered in 1989… We can then build our family trees surrounding this confirming the idea that it is mendelian. But its not like we have data going back hundreds of years as confirmation.

This part of our discussion begs the question of the validity and accuracy of our genetic tools, but we can save that discussion for another time.

What can we Learn?

So perhaps we have no choice that heredity plays a role in the cause of some of these diseases. But it must be questioned, how are these disorders showing up de novo so often and consistent? Why is it that these so called genetic disorders come about in the first place? I think the answers are in the work of Dr. Price. The health of the parents depicts the health of the children. Parental toxicity and deficiency can cause these perceived genetic disorders and give a semblance of heredity. This indicates that our genes do not contribute to or cause disease whatsoever.

Even if Mendelian diseases are purely caused by our genes, it would not follow logical order to induce that diseases outside of the mendelian family act in such a way. It is paramount that we understand from an ‘evolutionary’ or more accurately described, adaptive lens, that mendelian (or all genetic conditions) would not survive without modern medicine, which is a novel phenomenon.

Poor Science

Littered within the literature is poorly conducted and communicated science. Many of the claims that are made within the scope of genetics, are on the forefront of the pollution. The idea of genetic susceptibility, genetic and environmental interplay, the idea that genes fit into the causes of multifactorial disorders, genetic screening, as well as the aforementioned problems in detecting genetic variants/mutations. Genetics is the best scapegoat medicine and science has ever encountered!

Genetic susceptibility

To say that one is genetically susceptible is an unfalsifiable statement. How would one prove that there is susceptibility associated with the gene? If an individual, who has a gene that causes susceptibility, was symptomatic we say: Great! This confirms our theory! If that same individual was asymptomatic we say: Great! This confirms our theory! Either result fits the theory, which makes it unfalsifiable.

Genetic and Environmental Interplay

The complex interplay between our genes and the environment is a common phrase in medical research. It suggests that both genetic predispositions and external factors contribute to health and disease outcomes. For instance, it is said that certain gene variants can increase the risk of developing conditions like diabetes, but lifestyle choices such as diet and exercise can significantly modify this risk. If a disease requires environmental factors to manifest, the genes do not matter.

Think of it like planting a seed in dry, rocky soil. The seed (genes) has the potential to grow, but without water, sunlight, and nutrients (environmental factors), it won’t sprout or flourish. In this way, the genetic “potential” doesn’t matter if the necessary environmental conditions aren’t there to activate it.

Genetics and Multifactorial disorders

A multifactorial disorder is a health condition influenced by a combination of genetic, environmental, and lifestyle factors, rather than being caused solely by a single gene mutation. Examples include diseases like diabetes, heart disease, and certain types of cancer, where multiple genes and external influences contribute to the overall risk and manifestation of the disorder. But again, this entire idea relies on the unscientific and unfalsifiable idea of genetic susceptibility.

Genetic Modification

Some studies introduce a genetic modification into a mice for example to try to prove that the genetics are the cause or at least contribute to the disease. Take this study for example. This study created two rat models of cystic fibrosis (CF) by editing their genes—one with a common CF mutation and one missing the CFTR gene entirely. The control wild-type animals have the normal, unaltered CFTR gene, meaning they don’t carry any mutations associated with cystic fibrosis and have fully functional CFTR protein.

The results obviously show that the control experiences far less symptoms than the experimental group. However, this does not negate the fact that in the real world, something is triggering this genetic change. And just because we can go downstream and alter the genes directly to get an outcome, doesn’t mean that’s the way it works in real life.

If a mechanic puts worn down breaks on the car, the car wont stop properly. But in reality, breaks wear down over time, due to the environment of the car. To go further, the worn down breaks were designed to mimic the worn down breaks of another car.

Genetic Screening

The reality of genetic screening is that most individuals that have a gene linked with a certain disease don’t have, and will never have that illness. Let us, for example, take the BRCA genes associated with breast cancer.

You can have the BRCA genes and get cancer, or you could never develop cancer. You also don’t need to have the BRCA genes to get breast cancer.

Remember that most breast cancers happen by chance. Researchers estimate that only around 5 to 10 out of 100 breast cancers (5 to 10%) are caused by an inherited faulty gene.

Quote from cancer research UK.

To showcase the completely unscientific nature of the field of genetics in relation to disease, this study concludes the following:

For women with BRCA mutations who choose annual screening with MRI and mammography, the probability of dying of breast cancer within 20 years is 2%

But no control was used! We pull this statistic out of thin air, with no comparison.

Single Nucleotide Polymorphisms act in the same way. In fact, all claims that a gene, or multiple genes, contribute to a disease, act in this way. You can have the gene and be healthy, you can have the gene and have the disease, the gene can be absent and you can be healthy, the gene can be absent and you can be diseased. Once again, our genes do not contribute to or cause disease. Our genes are downstream of environmental factors.

Conclusion

A harsh conclusion, that is certainly an uncomfortable truth, is that our children’s diseases, of any kind, are directly the fault of their environment or ours as parents, both of which are the parents’ responsibility. The sad reality is that those that influence us most as parents, namely doctors, and thus the current scientific consensus hides the necessity of having a clean environment.

We use the scapegoat of genetics to hide the fact that WE are responsible for the disease in the world today. This consensus that our genes are largely the cause of autoimmune diseases, cancer, chromosomal disorders, chronic conditions of any kind, is extremely corrosive as it removes the responsibility from the establishments and governments to practice and govern in a manner conducive to healthy environments. We continue to allow low quality food, processed foods, pharmaceuticals, environmental toxins, etc. It is time to take responsibility and to nourish ourselves and our environments properly, while minimizing toxicities as well.