Genetics is everywhere. Genes contain all the information an organism uses to function (genotype) and they are handed down from parents to offspring. However, organism’s observable characteristics or traits (phenotype) depends from the combination of genetic processes with an organism’s environment and experiences that influence its development and behavior. Take two seeds of a genetically identical corn, place one seed in a temperate climate and one in an arid climate. Do you think they will grow in the same way? Although genetics would set the two plants to grow almost identically, the one in the arid climate only grows to half the height of the one in the temperate climate due to lack of water and nutrients in its environment. While current medicine mainly talks about genetic factors in many diseases, we should remember that man also is affected by environmental factors. So, what is the limit between the effect of genetics (nature) and environment (nurture) on humans? Is genetics really to blame for all the modern diseases? Read through and you will discover part of the truth.

Although genes contain all the information an organism uses to function, the environment plays an important role in determining the ultimate phenotypes an organism displays. Tropism in plants indicates the movement in response to an environmental stimulus [1]. In phototropism, shoots grow in the direction of the light source, since it is its main source of energy. In gravitropism, roots grow in the direction of gravitational pull (i.e., downward) and stems grow in the opposite direction (i.e., upwards, Figure 1). Also, in autotropism, proprioception is the ability of plants to perceive their own deformations, stimulating straightening of a curved organ.  In natural conditions, the three processes interact constantly.

Figure 1 – Example of gravitropism. (From [45])
Man is not different. Our parents give us the genetic traits, the growing path. This path is then followed or not depending on the environment. Take twins: sun exposure and smoking have an impact on facial appearance (Figure 2), with just a 5-year difference in smoking history producing noticeable differences in their faces [2].

Figure 2 – At age 61, identical twins Jeanne (on the left) and Susan no longer look exactly alike. Susan (on the right) smoked for many years and is an admitted sun worshipper, habits Jeanne does not share.(From [46])
Current medicine labels many diseases, disorders and syndromes with genetic etiology. However, many of them only spread in recent times. So, are we sure it is really genetic?

Malocclusion is one of these problems believed to be genetic. It is becoming so common in our modern society that almost everyone thinks having a brace is a step strictly required throughout our life. However, if we look to our ancestors (the origin of our genes), there is very little sign of malocclusion [3]. Figure 3 shows the difference of a prehistoric skull against a modern one: the difference in the palate shape and airways size is massive. So, is it really genetic?

Figure 3 – On the left, prehistoric skull: notice the large flat U-shaped palate and bigger airways. On the right, a modern skull with narrow high v-shaped palate and reduced airways. (From [3])
Luckily many doctors (John Mew and Weston A. Price among these) questioned the etiology of malocclusion, concluding that it is a consequence of poor craniofacial development: bones remodel according to force stimuli that in case of maxilla are primarily coming from the tongue and the teeth (through masseter muscle). Bottle-feeding, pacifiers, industrial soft high-calorie food, mouth breathing, too-early weaning  are common features of modern society determining the causes of jaw problems. Moreover, as usually happens with modern medicine, only symptoms are treated: when wearing braces, teeth are straightened but the underlying jaw problem is not resolved. This means either a retainer is needed for the rest of the life or the final result will relapse [4]. By instead treating the underlying problem, no relapse happens in the future, as in the case of patients treated by John Mew (Figure 4).

Figure 4 – Patient treated by John Mew with Orthotropics, by correcting the facial growth. Notice how correcting the jaw problem results in a correction of the malocclusion problem, with no future relapse.

Many other diseases are considered genetic, despite several clues supporting the opposite. Hair loss is one of these and it exponentially spreads in last decades. According to the current medicine, the typical male pattern baldness, characterized by hair on the sides and bald on top, depend on the miniaturization of genetically programmed hair follicles driven by activity of the dihydrotestosterone (DHT). Hair follicles on side would be genetically different and resistant to DHT action. But if this is true, why, once transplanted on the top, these terminal hair starts to fall again after some time, leaving patients as in Figure 5? And why vellus hair (miniaturized, balding) regenerates just as well as or even better than terminal hair (hairy, nonbalding) when transplanted in similar environments [5]?

Figure 5 – Head with hair loss and scar from hair transplant. (From [47])
The simple answer is that genetic plays a little role in male pattern baldness. Indeed, a poor craniofacial development leads to poor body posture with abnormal tension of neck muscles. This tension propagates to the galea aponeurotica (Figure 6) that tightens and compress blood vessels, causing fibrosis and calcification that further tighten the galea. Hypoxia (oxygen deficiency in the tissues) causes the death of hair follicles, thus hair loss. It is a confirmation the fact that blood flow in scalp of balding people is significantly lower than the one in normal people [6]. Furthermore, men suffering from androgenic alopecia have significantly lower oxygen partial pressure (meaning microvascular insufficiency and hypoxia) in the areas of their scalp affected by balding (frontal and vertex regions) versus unaffected areas (temporal and occipital regions) [7]. Also, by relieving tension at the vertex in the scalp, cutaneous blood flow rate increases, promoting hair regrowth [8,9].

Figure 6 – The galea aponeurotica is attached to the occipitofrontalis muscles and to the temporalis muscle via the temporalis fascia. Neck muscle tension propagates to the head, causing the galea to tighten, promoting loss of hair in the typical male pattern baldness. (From [48])
Poor body posture may be responsible for many other disorders. We have muscle chains that run throughout our body, tightening and compensating to maintain a stable posture, and bones that can twist or rotate, like in the case of vertebrae rotation. And there are blood vessels, nerves, glands, organs that can be compressed by either overtightened  muscles or by bones and vertebrae misalignment.

Stuttering is largely thought to be genetic. However, a recent research found out that people with stuttering have a lower regional cerebral blood flow in Broca’s area [10]. Is this genetic? Remember that we have large blood vessels going to the brain that can be compressed by neck muscle tension [11,12] and arteries that can be compressed by vertebral rotation [13,14,15]. Could be this also the cause of also many other syndromes arisen in modern times? Multiple Sclerosis has been linked to CCSVI (chronic cerebrospinal venous insufficiency) [16,17], that is a reduced blood flow from the brain and spinal cord due to narrowing of veins in the neck, in particular of the jugular veins. Patients with mild cognitive impairment, dementia and Alzheimer’s disease also show a reduced cerebral blood flow [18,19], with the entire brain that is degraded, resulting in tissue loss (Figure 7).

Figure 7 – Brain atrophy in advanced Alzheimer’s Disease. In an Alzheimer’s patient, the entire brain is degraded resulting in tissue loss. The cortex of the brain shrivels up, which damages the ability of the brain to think, plan, and remember. (From [49])
Carpal tunnel syndrome is the disability that results from the median nerve being pressed or squeezed, causing numbness, tingling, or burning sensations in the thumb and fingers, with pain in the wrists or hands, loss of grip strength and loss of manual dexterity. The major risk factor for carpal tunnel syndrome is considered genetic. However, poor body posture, especially in cases of forward head posture, implies protracted shoulders, increasing strain on the various nerves passing through the shoulder region. One of these nerves is indeed the median nerve. Did you know that carpal tunnel syndrome is associated with forward head posture [20]?

Figure 8 – There are two main nerves that service the arm, the median and the ulnar nerves. Both flow out from the neck and make their way down through the upper extremity. Carpal tunnel syndrome derives from median nerve compression in the shoulder area. (From [50])
In many cases of TMJ internal derangement, the auriculotemporal nerve (a small branch of the mandibular nerve) can become drawn into the compression zone of the TMJ, with possible neuroinflammation. This neuroinflammation may spread and could act as physiological drivers for aberrant reflexive behaviors, arising movement disorders, e.g. dystonia, Tourette’s syndrome [21,22]. Being the TMJ in direct relationship with the cranial structure and body posture, many other disorders are linked to TMD, such as fibromyalgia [23] and multiple sclerosis [24].

Genetics is also considered to play an important role in obesity. As Figure 9 shows, obesity has been linked with an increased risk of developing insulin resistance and type 2 diabetes [25], increased risk of hypertension [26] and cardiovascular disease (e.g. heart failure, coronary heart disease, sudden cardiac death) [27], cancer [28], mental disorders [29] and higher mortality [30,31].

Figure 9 – Co-morbidities associated with overweight and obesity. (From [32])

If you believe that all of this is related to bad genes, then it is better that you reconsider your thoughts: remission of type 2 diabetes comes from changing dietary and physical activity habits [33]; healthy food can reduce hypertension by 21 mmHg (drugs usually reduce it by 10-15 mmHg) [34,35]; fruit and vegetables have a strong protective effect against cardiovascular diseases [36,37], cancer [38,39] cognitive decline [40,41] and all-cause mortality [42,43]; increased consumption of whole grains has been associated with reduced risk of major chronic diseases including cardiovascular disease, type II diabetes, and some cancers [44].

So, is genetic really to blame for many modern syndromes? This article has not been written with the purpose of voiding genetic factors in the etiology of many diseases. Genetics is present in everything. The purpose of this article is trying to educate people in the pursuit of the truth, giving emphasis to the environmental causes that have been widely suppressed, hidden or forgotten by the current medicine. Remember that there is always a reason for everything!



[1] Bastien, Renaud, Stéphane Douady, and Bruno Moulia. “A unified model of shoot tropism in plants: photo-, gravi-and propio-ception.” PLoS computational biology 11.2 (2015): e1004037.

[2] Okada, Haruko C., et al. “Facial changes caused by smoking: a comparison between smoking and nonsmoking identical twins.” Plastic and reconstructive surgery 132.5 (2013): 1085-1092.

[3] Boyd, Kevin L. “DARWINIAN DENTISTRYPART.” Journal of American Orthodontic Society (2012): 28-33.

[4] Steinnes, Jeanett, Gunn Johnsen, and Heidi Kerosuo. “Stability of orthodontic treatment outcome in relation to retention status: An 8-year follow-up.” American Journal of Orthodontics and Dentofacial Orthopedics 151.6 (2017): 1027-1033.

[5] Krajcik, Rozlyn A., et al. “Transplants from balding and hairy androgenetic alopecia scalp regrow hair comparably well on immunodeficient mice.” Journal of the American Academy of Dermatology 48.5 (2003): 752-759.

[6] Klemp, Per, Kurt Peters, and Birgitte Hansted. “Subcutaneous blood flow in early male pattern baldness.” Journal of investigative dermatology 92.5 (1989): 725-726.

[7] Goldman, Boris E., David M. Fisher, and Steven L. Ringler. “Transcutaneous PO2 of the scalp in male pattern baldness: a new piece to the puzzle.” Plastic and reconstructive surgery97.6 (1996): 1109-16.

[8] Freund, Brian J., and Marvin Schwartz. “Treatment of male pattern baldness with botulinum toxin: a pilot study.” Plastic and reconstructive surgery 126.5 (2010): 246e-248e.

[9] Toshitani, Shoji, et al. “A New Apparatus for Hair Regrowth in Male‐pattern Baldness.” The Journal of dermatology 17.4 (1990): 240-246.

[10] Desai, Jay, et al. “Reduced perfusion in Broca’s area in developmental stuttering.” Human brain mapping 38.4 (2017): 1865-1874.

[11] Gray, Sarah Delcenia, Erik Carlsson, and Norman C. Staub. “Site of increased vascular resistance during isometric muscle contraction.” American Journal of Physiology–Legacy Content213.3 (1967): 683-689.

[12] TOOLE, JAMES F., and SAMUEL H. TUCKER. “Influence of head position upon cerebral circulation: studies on blood flow in cadavers.” AMA Archives of Neurology 2.6 (1960): 616-623.

[13] Zaina, C., et al. “The effect of cervical rotation on blood flow in the contralateral vertebral artery.” Manual Therapy 8.2 (2003): 103-109.

[14] Mitchell, Jeanette, et al. “Is cervical spine rotation, as used in the standard vertebrobasilar insufficiency test, associated with a measureable change in intracranial vertebral artery blood flow?.” Manual Therapy 9.4 (2004): 220-227.

[15] Mitchell, Jeanette. “Vertebral artery blood flow velocity changes associated with cervical spine rotation: a meta-analysis of the evidence with implications for professional practice.” Journal of Manual & Manipulative Therapy 17.1 (2009): 46-57.

[16] Zamboni, Paolo, et al. “Chronic cerebrospinal venous insufficiency in patients with multiple sclerosis.” Journal of Neurology, Neurosurgery & Psychiatry 80.4 (2009): 392-399.

[17] Al-Omari, M. H., and L. A. Rousan. “Internal jugular vein morphology and hemodynamics in patients with multiple sclerosis.” International Angiology 29.2 (2010): 115.

[18] Dai, Weiying, et al. “Mild cognitive impairment and alzheimer disease: patterns of altered cerebral blood flow at MR imaging.” Radiology 250.3 (2009): 856-866.

[19] Rogers, Robert L., et al. “Decreased cerebral blood flow precedes multi‐infarct dementia, but follows senile dementia of Alzheimer type.” Neurology 36.1 (1986): 1-1.

[20] De-La-Llave-Rincón, Ana I., et al. “Increased forward head posture and restricted cervical range of motion in patients with carpal tunnel syndrome.” journal of orthopaedic & sports physical therapy 39.9 (2009): 658-664.

[21] Sims, Anthony B., Vincent P. Clark, and Mark S. Cooper. “Suppression of movement disorders by jaw realignment.” Pain Medicine 13.5 (2012): 731-732.

[22] Sims, Anthony B., Brendan C. Stack, and G. Gary Demerjian. “Spasmodic torticollis: the dental connection.” CRANIO® 30.3 (2012): 188-193.

[23] Plesh, Octavia, Frederick Wolfe, and Nancy Lane. “The relationship between fibromyalgia and temporomandibular disorders: prevalence and symptom severity.” The Journal of rheumatology 23.11 (1996): 1948-1952.

[24] Badel, Tomislav, et al. “Temporomandibular joint disorder in a patient with multiple sclerosis–review of literature with a clinical report.” Collegium antropologicum 34.3 (2010): 1155-1159.

[25] Kahn, Steven E., Rebecca L. Hull, and Kristina M. Utzschneider. “Mechanisms linking obesity to insulin resistance and type 2 diabetes.” Nature 444.7121 (2006): 840.

[26] Rahmouni, Kamal, et al. “Obesity-associated hypertension: new insights into mechanisms.” Hypertension 45.1 (2005): 9-14.

[27] Hubert, Helen B., et al. “Obesity as an independent risk factor for cardiovascular disease: a 26-year follow-up of participants in the Framingham Heart Study.” Circulation 67.5 (1983): 968-977.

[28] McCann, Jean. “Obesity, cancer links prompt new recommendations.” Journal of the National Cancer Institute93.12 (2001): 901-902.

[29] Simon, Gregory E., et al. “Association between obesity and psychiatric disorders in the US adult population.” Archives of general psychiatry 63.7 (2006): 824-830.

[30] Masters, Ryan K., et al. “The impact of obesity on US mortality levels: the importance of age and cohort factors in population estimates.” American journal of public health 103.10 (2013): 1895-1901.

[31] Adams, Kenneth F., et al. “Overweight, obesity, and mortality in a large prospective cohort of persons 50 to 71 years old.” New England Journal of Medicine 355.8 (2006): 763-778.

[32] Kyrou, Ioannis, Harpal S. Randeva, and Martin O. Weickert. “Clinical problems caused by obesity.” (2014).

[33] Lean, Michael EJ, et al. “Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial.” The Lancet (2017).

[34] Juraschek, Stephen P., et al. “Effects of sodium reduction and the DASH diet in relation to baseline blood pressure.” Journal of the American College of Cardiology 70.23 (2017): 2841-2848.

[35] Appel, Lawrence J. “ASH position paper: dietary approaches to lower blood pressure.” Journal of the American Society of Hypertension 4.2 (2010): 79-89.

[36] Ness, Andrew R., and John W. Powles. “Fruit and vegetables, and cardiovascular disease: a review.” International Journal of epidemiology 26.1 (1997): 1-13.

[37] Bazzano, Lydia A., et al. “Fruit and vegetable intake and risk of cardiovascular disease in US adults: the first National Health and Nutrition Examination Survey Epidemiologic Follow-up Study.” The American journal of clinical nutrition76.1 (2002): 93-99.

[38] Block, Gladys, Blossom Patterson, and Amy Subar. “Fruit, vegetables, and cancer prevention: a review of the epidemiological evidence.” Nutrition and cancer 18.1 (1992): 1-29.

[39] Steinmetz, Kristi A., and John D. Potter. “Vegetables, fruit, and cancer prevention: a review.” Journal of the american dietetic association 96.10 (1996): 1027-1039.

[40] Loef, Martin, and Harald Walach. “Fruit, vegetables and prevention of cognitive decline or dementia: a systematic review of cohort studies.” The journal of nutrition, health & aging 16.7 (2012): 626-630.

[41] Solfrizzi, V., F. Panza, and A. Capurso. “The role of diet in cognitive decline.” Journal of neural transmission 110.1 (2003): 95-110.

[42] Steffen, Lyn M., et al. “Associations of whole-grain, refined-grain, and fruit and vegetable consumption with risks of all-cause mortality and incident coronary artery disease and ischemic stroke: the Atherosclerosis Risk in Communities (ARIC) Study.” The American journal of clinical nutrition 78.3 (2003): 383-390.

[43] Wang, Xia, et al. “Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose-response meta-analysis of prospective cohort studies.” Bmj 349 (2014): g4490.

[44] Okarter, Neal, and Rui Hai Liu. “Health benefits of whole grain phytochemicals.” Critical reviews in food science and nutrition50.3 (2010): 193-208.

Other websites

[45] Plants Tropisms, by Richard D Firn

[46] Study of identical twins reveals how habits like smoking and tanning can dramatically age skin, by Daily News

[47] Repair: Old Plug Removal, SMP Into Hair Transplant Scar, by Balding Blog

[48] Muscles Of The Face Diagram, by Anatomy Human

[49] Alzheimer’s: Never a Dull Moment

[50] Carpal Tunnel Syndrome and the Median Nerve, by Corewalking