Hair growth and the fluid factor

Hair growth and the fluid factor

Medical Hypotheses Medical Hypotheses(1995) 44, 475-478 © Pearson Professional Ltd 1995 Hair Growth and the Fluid Factor S. I. FOOTE 5 Chiltern Avenu...

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Medical Hypotheses Medical Hypotheses(1995) 44, 475-478 © Pearson Professional Ltd 1995

Hair Growth and the Fluid Factor S. I. FOOTE 5 Chiltern Avenue, Macclesfield, Cheshire, Skl 1 8LP, UK

Abstract - - It is accepted that the detailed mechanisms of changes in human hair growth patterns are poorly understood. It is this uncertainty that has encouraged many charlatans to operate in this area. From my perspective as an engineer, however, there is a simple mechanism that makes sense of these changes. I suggest this mechanism is closely connected with the evolution and function of hair. The fact that the presence of this mechanism can be demonstrated in the male pattern baldness scenario, raises a number of serious questions relating to fundamental physiology and the mechanisms of some serious diseases. As an amateur, it is difficult for me to gain access to up-to-date research data, so my references are derived from textbooks. I would therefore welcome comments from professionals who are involved in the areas indicated in this paper.

Introduction

Although hair loss is known to be associated with certain factors, e.g. male hormones, immune system disorders and toxic effects such as chemotherapy, the mechanisms of these changes are not adequately explained. For example, the contrary effects that male hormones have in increasing body hair growth whilst at the same time reducing scalp hair growth are placed in the 'catch all' area of genetic or hereditary effects (1). This assumption of genetic influences arises largely because transplanted hair continues to grow in bald areas. I would suggest however that there is a simple factor that explains this form of hair loss, and indicates a common factor in most incidences of hair loss and, indeed, hair growth. The only consistent observations are that changes in hair production are associated with changes in the shape and size of hair follicles. The known hair cycle demonstrates the regular breakdown and redevelopment of the hair bulb at the base of the follicle. The

length of the anagen growth phase and the area of the hair bulb during this period determine hair production. Hair loss is associated with follicle shrinkage and involution of the hair bulb. Both hair follicles and their associated sebaceous glands are known to increase production when they enlarge however. The expansion and contraction of hair follicles and sebaceous glands can be easily explained when you consider that both are hollow structures surrounded by soft tissue. Any expansion of this tissue would automatically shrink these hollow structures; conversely, any shrinkage of soft tissue would enlarge them. This simple connection is the key to making sense of most changes in human hair patterns. The mechanisms of tissue expansion and contraction are well documented, and once the relationship with hair is understood, it is difficult to dispute the evidence for this connection. The production area of the hair bulb is formed by the dermal papilla protruding into the base of the main

Date received 31 August 1994 Date accepted 28 December 1994

475

476 tubular section of the follicle. This tubular section is a down growth of the skin (2), and the dermal papilla lies in tissue that is a 'distance' below the skin's surface. If the soft tissue around the follicle begins to expand, the surface of the skin moves away from the dermal papilla pulling the tubular section of the follicle with it. The hair bulb becomes involute. Any existing hair is peeled away by this action and shed. Shrinkage of this soft tissue moves the follicle's tubular section towards the dermal papilla. This allows the development of a larger, more productive hair bulb during the anagen growth phase. There are a number of factors that influence both the degree of tissue expansion and contraction, and the movement this creates in the follicle. 1. The production area of the follicle under normal conditions; 2. The overall length of the follicle. Any movement in soft tissue will cause more relative movement in longer follicles. Short follicles are more resistant to tissue movement; 3. The tissue fluid pressure; 4. The resilience of the tissue in the area of the follicle. This will govern the amount of tissue movement for a given change in tissue fluid pressures. The only variable factor here is the tissue fluid pressure.

Evolution I believe the evidence to be that the structure of hair follicles and sebaceous glands has evolved around the characteristics of surface tissue in order to integrate hair with the bodies other temperature control systems. In mammals, blood supply and tissue fluid levels reduce in response to low temperatures (3). This is why ice-packs are used to reduce inflammation around injuries. In hairy mammals, a reduction in environmental temperature shrinks the surface tissue. Hair follicle production areas increase, particularly in longer follicles. Sebum production also increases, and the result is a winter coat. As temperatures rise, blood supply to surface tissue increases. Tissue expands and the animal moults. This 'hydraulic' mechanism has other important benefits. Any tissue damage will trigger the inflammatory response (4). Localised tissue expansion shuts down any follicles in the area and hair recedes away from the wound. This enables cleaning to be more effective and significantly reduces the chances of serious infection. Once inflammation subsides, hair growth resumes.

MEDICAL HYPOTHESES

Human hair patterns If you list the conditions that are known to involve a degree of hair loss, all these conditions also involve excess tissue fluid level via inflammation or oedema: 1. Hormonal action, for example pregnancy, myxoedema; 2. Malnutrition; 3. Some types of kidney disease; 4. The so called auto-immune conditions; 5. Exposure to radiation; 6. Chemotherapy; 7. Toxic effects; 8. Infections; 9. Physical trauma; 10. Shock. The currently known treatments that improve hair growth, have the common action of moving fluid. The drug minoxidil (Upjohn Company) is currently the only recognised, effective treatment for male pattern baldness. This drug was developed for hypertension, i.e. it effects the body's fluid system. Steroid antiinflammatories are known to be effective against hair loss in women. I would suggest that electrolysis and massage operate the lymphatic 'pump'. Current treatments for hair loss are not very effective. Understanding this mechanism is the key to developing better treatments. When hair is transplanted as plugs of tissue, the initial inflammatory response creates hair loss in both graft and surrounding tissue. After healing, the grafts become subject to the same conditions as surrounding tissue. However the hard scar tissue reinforces the graft against further expansion. When you examine these grafts after a period of time, you notice that hair is more abundant near the edges, i.e. near the scar. Often there is some distortion of productive follicles in the grafts, and this creates wavy hair growth. Any further expansion of surrounding tissue leaves the grafts as pits in the scalp (personal observation).

Hormonal effects It is well known that hormone activity is responsible for the development of the different hair patterns of the sexes. This increased hormone activity at puberty causes many changes. It is responsible to hypothesise that this growth process includes increases in nutrient transport efficiency. In this respect, increased lymphatic drainage efficiency would be beneficial. I think the layout of the lymphatic drainage system in the

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HAIR GROWTH AND THE FLUID FACTOR

body speaks volumes for changes in human hair patterns (5). The hydraulic hair mechanism and its associated factors are present in most human hair pattern scenarios. If you examine the tissue beneath the eyebrows, it feels thin. I would suggest that negative tissue fluid pressures easily shrink this tissue and produce eyebrow growth. The particular male hormone responsible for male hair patterns is known. Dihydrotestosterone (DHT), is formed by enzyme action upon testosterone and is known to be responsible for (6): 1. 2. 3. 4. 5.

Facial hair growth; Body hair growth; Increased sebum production; Scalp hair loss; Enlargement of the prostate gland.

All these effects are consistent with changes in tissue fluid levels. The evidence is that DHT acts via the lymphatic system to increase tissue drainage significantly. The area of fluid dynamics is full of examples of one action creating opposite effects. A good analogy of the action of DHT is the removal of the radiator restrictors in a central heating system. These exist to balance the flow through the system. If these restrictors are removed, hot and cold areas develop in accordance with the plumbing characteristics. I suggest that DHT removes the restrictors. The scalp area is at the end of the head' s lymphatic system, and the prostate is known for being a poor drainage area (7). If a general improvement in tissue fluid turnover complements the action of testosterone, evolution would retain the characteristic, especially when this involves an increase in available reproductive fluid. The pattern created in this form of scalp hair loss can be easily explained by the hydraulic mechanism and associated factors. You can often see the point low on the forehead where the swelling starts. As this expansion extends upwards, hair starts to recede. A close examination of bald tissue indicates how smooth the skin is, as it is stretched taut by expansion of underlying soft tissue. This is why people often refer to a shiny bald head. You can demonstrate tissue expansion in male pattern baldness with the normal pitting oedema test (8). If you treat the area with minoxidil (Upjohn Company) you can observe the development of fine wrinkles in the skin (personal observation). This crazing effect precedes any improvement in hair growth in previously thin areas and demonstrates the shrinkage of underlying soft tissue.

The demonstrable presence of this mechanism in this scenario has serious implications.

The fluid factor and disease The concept of a general difference in tissue fluid levels between the sexes, and localised differences in the individual fits in very well with the known incidence of certain diseases. The use of DHT in fluid adjustment therapy may prove beneficial in the prevention and treatment of these diseases. Changes in tissue fluid characteristics influence both the immune response and tissue cell proliferation. The suppression of inflammation inhibits both these processes (9). It is reasonable to hypothesise, therefore, that excess fluid may encourage these processes. In reducing fluid levels, DHT could be responsible for the reduced incidence of inflammatory related conditions in men, for example rheumatoid arthritis (10). At present, corticosteroids are the most effective treatment for this type of condition. These hormones also reduce fluid levels and promote hair growth (11). Corticosteroids, however, have dangerous side-effects. DHT may have the required therapeutic effect, without the side-effects of corticosteroids. There are many processes that influence cell proliferation, but I would suggest that normally available space will overrule these processes. The inflammatory response to injury triggers cell multiplication. Once the space is filled, this multiplication stops (12). An increase in extra-cellular space due to high fluid levels could encourage proliferation of certain cell types. In fact, this would be a convenient way of building a tissue. However, this increased cell division and multiplication may in turn create a greater risk of cell mutation and malignancy, This scenario indicates close similarities in the physiology of the male prostate and the female breast. Both glands are known saturated areas, and are subject to tissue thickening or benign enlargement, both glands are also prone to malignancy. It is known that prostate cancer is almost certainly associated with benign enlargement (13). Oestrogen is suspected of having a role in the development of certain cancers~ As in the known risk of hormone replacement therapy (14) and breast cancer (15), oestrogen is also known to promote fluid retention (16) and hormone level fluctuations are known to cause changes in the fluid level of breast tissue (17). This indicated relationship between tissue development and fluid characteristics could account for the abnormal tissue development in males with congenital deficiency of DHT (18).

478 In conclusion, at the very basic level, any organism is a group of cells and a nutrient transport system. The hydraulic mechanism of hair growth, offers a major opportunity for further understanding of this interrelationship, evolution and the mechanisms of disease.

References 1. Ganong W F. Review of Medical Physiology, 16th edn. Hemelhemstead: Appleton and Lange, 1993: 392-393. See also Hinchcliff S, Montague S. Physiology for Nursing Practice. London: Bailli&e Tindall, 1991: 560. 2. Hinchcliff S, Montague S. Physiology for Nursing Practice. London: Baillitre Tindall, 1991: 558. 3. Hinchcliff S, Montague S. Physiology for Nursing Practice. London: Bailli~re Tindall, 1991: 550, 569. 4. Hinchcliff S, Montague S. Physiology for Nursing Practice. London: Bailli~re TindaU, 1991: 574. 5. Hinchcliff S, Montague S. Physiology for Nursing Practice. London: Ballli~re Tindall, 1991: 596.

MEDICALHYPOTHESES 6. Hamand J. Prostate Problems. London: Thorsons, 1991: 90-91. 7. Hamand J. Prostate Problems. London: Thorsons, 1991: 107-108. 8. Hinchcliff S, Montague S. Physiology for Nursing Practice. London: Baillitre Tindall, 1991: 564. 9. Hinchcliff S, Montague S. Physiology for Nursing Practice. London: Bailli~re Tindall, 1991: 194-195,574-576. 10. Inglis J K. A Textbook of Human Biology, 3rd edn. Oxford: Pergamon Press, 1986:313. 11. Inglis J K. A Textbook of Human Biology, 3rd edn. Oxford: Pergamon Press, 1986: 240. 12. Hinchcliff S, Montague S. Physiology for Nursing Practice. London: Baillitre Tindall, 1991: 575-576. 13. Hamand J. Prostate Problems. London: Thorsons, 1991: 133. 14. Hinchcliff S, Montague S. Physiology for Nursing Practice. London: Balllitre Tindall, 1991: 626. 15. Hinchcliff S, Montague S. Physiology for Nursing Practice. London: Baillitre Tindall, 1991: 636. 16. Hamand J. Prostate Problems. London: Thorsons, 1991: 141. 17. Hinchcliff S, Montague S. Physiology for Nursing Practice. London: Bailli~re Tindall, 1991: 622. 18. Ganong W F. Review of Medical Physiology, 16th edn. Hemel Hempstead: Appleton and Lange, 1993: 393.