Barriers to Disease
2.1a Health and susceptibility: what makes us vulnerable to disease?
In this first half of Stage 2 there is a progression from the introductory topics of Stage 1 to an exploration of the foundations of pathology, the study of how the body responds to disease. We begin with a discussion of the concept of susceptibility to disease.
Susceptibility as vulnerability to disease
In Section 1.1e the basic causes of disease from the perspective of both conventional and more holistic approaches to medicine were introduced. This section explores the topic of causation of disease in more detail, and in particular, which factors influence susceptibility to disease. Susceptibility is used commonly in conventional medicine to refer to vulnerability to disease. From a holistic perspective, susceptibility might more accurately be defined as vulnerability to imbalance, as within a holistic paradigm, including that of Chinese medicine, reduced health tends to be considered in terms of patterns of imbalance rather than as disease.
Conventional view of barriers to disease
Conventional medicine considers susceptibility in terms of weakness of one or more of a series of levels of defenses, or barriers to disease. This concept is highly suggestive of the prevailing view that the body is a fortress and disease an invading enemy. The body is understood to have several methods of protection against disease. Some of these are located in the superficial layers of the body, within the skin and mucous membranes, and others offer their protective action from within the deeper levels of the tissues beneath the skin and also from within the organs themselves.
Conventional medicine recognizes mechanical and immune barriers to disease. Mechanical barriers are those that confer protection as a result of the physical structure of the barrier (e.g. the keratinized squamous epithelium of the skin). Immune barriers are those that protect by means of a complex interaction of the immune cells and proteins (including antibodies) that circulate in the body fluids and can move into tissues when required. Table 2.1a-I summarizes those parts or functions of the body that have a protective role.
Name of barrier
Superficial protective barriers
Skin, and body hair
Oily secretion of skin (sebum)
Antibodies in sweat
The structures that protect the orifices (e.g. eyelids, nostrils, urethra)
Mucus secreted from mucous membranes
Antibodies in mucus and tears
Ability of wounds to heal
Ability of blood to clot
Deep protective barriers
Cushioning of subcutaneous tissues (fat)
Supportive and protective nature of other types of connective tissue in all parts of the body
Ability of wounds to heal
Ability of blood to clot
Immune cells and antibodies in the blood and lymph
Most of the mechanical barriers serve as a protective method for the body literally by providing physical protection against damage. For this reason healing of wounds and the blood-clotting mechanism have been classified as a mechanical barrier, even though a chain of physiological and chemical responses has to be set in action for them to exert their protective effect. The role of the immune system in protection is even more complex, as it involves the interaction of specialized white blood and other immune cells with substances identified as foreign that are located in the fluid components of the body. Wound healing, blood clotting and the immune system are each discussed in more detail in the following sections.
Health and susceptibility
Overarching the specific protection that the deep and superficial barriers to disease provide is the protection conferred by the general health of the body. Healthy function of any organ or body part will in itself provide a barrier against disease. For example, a perfectly structured heart organ will be less susceptible to heart disease than one with damaged heart valves or a weakness in the heart muscle. A failing organ will be more susceptible to further damage, and this is more likely to become a negative cycle of increasing disease.
In ill health susceptibility is increased because one or more of the barriers to disease will not be functioning as they should. The susceptibility that results from ill health can be categorized as either congenital (dating from the time of birth) or acquired (developing at a later stage in life as a result of deficiency, disease or injury).
Examples of congenital disease conferring susceptibility to progressive disease include albinism, hemophilia and congenital heart disease. In albinism an inability to produce the skin pigment melanin leads to vulnerability to sunburn and skin cancer and visual impairment. In hemophilia an inability to produce sufficient blood-clotting proteins leads to vulnerability to bleeding into joints and muscles. In congenital heart disease poorly formed heart valves and gaps in the internal muscle wall of the heart lead to vulnerability to poor heart pumping action, breathlessness and, over time, lung damage. The important congenital diseases are described in more detail in Section 5.4c.
Some forms of congenital susceptibility are more subtle. Although a named inherited condition, such as cystic fibrosis, may not be present, it is clear that some people fall ill more often than others, and for some, this has been the case since infancy. The term weak constitution might be applied in such a situation. This will be because the inherited barriers to disease are not as strong as they could be, but the impairment is not so specific as to constitute a named disease.
Acquired susceptibility is the consequence of a weakening of the barriers to disease after birth. Any one of the conventionally accepted causes of disease (Section 1.1e), such as poor diet, lack of exercise, obesity and smoking, will contribute to increased susceptibility well before disease has developed. For example, a long-term smoker may appear to be very fit but is, in fact, very likely to have sustained damage to a number of the barriers to disease, meaning that they have a higher risk of succumbing to disease. Reasons for this include the fact that smoking damages the protective lining of the lungs, so lung infections are more likely to take hold, and also that it impairs the free circulation of blood and increases the tendency of the blood to clot, which means that diseases of the cardiovascular system such as heart attack are more likely to occur. However, the fact that some smokers do not develop smoking-related diseases tells us that susceptibility is not the same as disease.
A smoker will always increase their risk of developing smoking-related disease by smoking because cigarette smoke invariably damages the lungs and circulation to some degree. If the smoker’s constitution is strong, the damage from smoking may not be so severe as to lead to a very high risk of disease, even though the personal risk of disease has undoubtedly increased. A person with an established impairment of the function of the lungs or circulation (e.g. someone with asthma or diabetes) already has an increased risk of developing lung and heart disease. The risk of these diseases therefore becomes even higher if such a person smokes.
Nevertheless, both types of smoker may avoid disease as other factors may be present that reduce susceptibility. For example, in the case of smokers, living in a warm, dry climate may reduce the risk of bronchitis, and eating a healthy, low-fat diet may reduce the risk of circulatory problems. Such factors are known as protective factors. Some protective factors may be far less easy to assess clinically than others – for example, personality traits such as a generally positive attitude or a calm approach to the vicissitudes of life may well be protective against illness.
Periods of naturally increased susceptibility
There are also times within a healthy lifespan when the barriers to disease are less effective. These can be seen as periods of naturally increased susceptibility to disease. Three significant periods when a healthy individual is more than usually susceptible to disease are infancy, pregnancy and old age. In infancy the barriers to disease such as the immune system or the ability to maintain a steady body temperature are not fully mature. In pregnancy the vitality required to maintain the healthy barriers to disease is diverted to the growing fetus (e.g. calcium is diverted to the fetus and the mother’s teeth become more vulnerable to decay) and also the rapid and significant changes to the structure and function of a pregnant woman’s body can in themselves lead to disease (e.g. hypertension of pregnancy, gestational diabetes, varicose veins and low back pain). In old age, all barriers to disease are in a state of degeneration (e.g. the skin and bones become less strong and are more vulnerable to damage by trauma).
The term risk factor is used medically to describe anything that increases the risk of disease. For example, high blood pressure is a risk factor for stroke, and unprotected sex is a risk factor for developing human immunodeficiency virus (HIV) infection.
Therefore, the presence of a risk factor means that the susceptibility to disease is increased. In fact, any of the conventional external causes of disease (e.g. inadequate diet, insufficient exercise, exposure to radiation and smoking) can also be seen as risk factors for disease.
Conventional doctors aim to reduce risk factors in order to prevent disease. Preventive medicine therefore aims to decrease susceptibility to disease.
Disease prevention may be directed at an individual patient, in the form of personalized health education advice, screening for early signs of preventable disease, or by prescribing medication to reduce the impact of risk factors such as high blood pressure. Alternatively, changes can be instituted at a community-based, national or even international level to prevent disease. Such changes may require political reform. The advances in sanitation in the UK made in the 19th century are an example of this sort of wide-scale public health measure. Other examples include legislation concerning the advertising of tobacco products, and supplementation of foods with nutrients, such as folic acid in breakfast cereals. Table 2.1a-II lists some more examples of approaches to the prevention of disease.
Table 2.1a-II Examples of preventive measures against known risk factors for disease
Information to the public about warning signs of meningitis to enable early recognition of cases
Antibiotics prescribed to close contacts of the person with the disease
Education campaign about safe sex
Free condoms at family planning clinics
Chlamydia infection screening programs
Education about healthy eating
Provision of healthy foods in schools
Government subsidies of healthy foods
Encouragement to exercise by providing cheap access to leisure centers, cycle tracks, etc.
Workplace policies to encourage staff to exercise
Tendency to accidents in childhood
Education of parents about risks
Safe play area and school environments
Promotion of safety measures in the home: smoke alarms, stairgates, etc.
Stop smoking campaigns
Prescription of nicotine patches
Legislation to control tobacco advertising and packaging
Taxation of tobacco products
Restriction on the sale of alcohol to children
Taxation of alcohol
2.1b Barriers to disease: wound healing
The role of wound healing and clotting1
The processes of wound healing and clotting were introduced in Section 2.1a as two of the mechanical barriers to disease. Unlike more structural barriers such as the skin or bony skeleton, these are both dynamic processes that are set in motion after injury has occurred. They prevent the damage from worsening, and enable repair to take place. In this way, their role is similar to that of the immune system.
The physiology of wound healing2
A description of the mechanism of wound healing is fundamental to a full understanding of how the body responds to disease. There are many situations in disease when the healthy structure of the body tissues is damaged and has to be repaired by means of this delicate process. The formation of a blood clot is the first stage of wound healing, and this is described in more detail in Section 2.1c.
Wound healing is least complicated when the injury is clean and there has been a simple cut or puncture to the tissue rather than a loss of tissue. With a clean cut or a puncture the edges of the wound can stay in alignment with each other, and if this ideal is enabled (e.g. by sutures or sterile adhesive tape strips), this provides the conditions for the process known as primary wound healing (or healing by first intention). If there has been loss of skin and underlying tissue, the wound healing has to fill and repair a gaping hole. The reparative process is more complex, takes longer and is prone to complications resulting from trauma and infection. This is known as secondary wound healing (or healing by second intention).
Primary wound healing
Primary wound healing can take place when the edges of a cut or puncture are in close opposition (see Figure 2.1b-I).
Figure 2.1b-I The stages of primary wound healing (healing by first intention)
Figure 2.1b-I illustrates the three stages of primary wound healing after a neat laceration to the skin. The laceration in this image only just penetrates the dermis of the skin, which means it is very superficial. The edges of the wound ooze blood from the broken capillaries, and the blood rapidly forms into a clot in the confined space. The blood clot releases messenger chemicals that stimulate the process of chemotaxis, the attraction of the cells of the immune system (the leukocytes) and the fibroblasts (the connective tissue repair cells) into the region of the clot. The phagocytic (engulfing) leukocytes move into the clot and absorb and remove cell debris, dirt and bacteria. Fibroblasts lay down a delicate network of fibrous strands that begin to bridge the gap formed by the wound. Into this meshwork the broken ends of the capillaries start to grow a new network of tiny vessels so that this developing scar tissue has a rich blood supply. At the same time, the deepest layer of the epithelium of the broken skin grows through the upper regions of the blood clot to close the breach formed by the injury. This stage is one of proliferation, and when the fibrous and capillary network is sufficiently strong, it causes the scab, the dried blood clot overlying the wound, to drop away, leaving the pink and delicate scar tissue protected by a layer of new epithelium beneath. The proliferative stage takes between 5 and 30 days depending on the size of the wound and the health of the patient. Over the next few days to weeks (the maturation phase) the delicate scar tissue becomes strengthened and more organized as a result of increasing amounts of fibrous tissue. The initially complex network of tiny capillaries is simplified in this phase. At the end of this phase what remains is a stronger, more densely structured and pale tissue than the newly formed scar.
Secondary wound healing
Secondary wound healing is the process that takes place when the wound leaves a gap in both the skin and the underlying connective tissue. Figure 2.1b-II illustrates the three stages of secondary wound healing. As is the case with primary wound healing, the first stage is the lining of this breach with a blood clot originating from blood that has oozed from the remaining damaged tissue. The clot encourages the ingrowth of new fibrous tissue and capillaries and the appearance of phagocytic cells to remove debris and bacteria. This delicate new tissue is known as granulation tissue. This proliferative stage takes longer than the corresponding stage in primary wound healing, the time to healing being dependent on the size of the breach in the tissue, and the health and quality of blood supply to the underlying tissue. If foreign bodies (dirt) and bacteria are present they can be the focus for ongoing damage, and will further slow this stage of the healing process. The initially shallow layer of proliferating new tissue cannot yet be lined by the epithelium and, once the scab drops away, it is covered by a moist yellowing layer of dead cells called slough. Like the old blood clot, slough continues to be a stimulus for the chemotaxis of fibroblasts, leukocytes and new capillaries. Once the new scar tissue reaches the level of the edges of the broken skin epithelium, the new epithelium can grow inwards, closing the breach by degrees. Any breach in an epithelium is called an ulcer, which means that secondary wound healing always involves the formation of an ulcer. Ideally, the ulcer is gradually reduced in size until it is has been closed over entirely by new epithelium. Following the closure of the ulcer the maturation phase continues to strengthen and organize the new fibrous tissue until the healed wound eventually appears as a pale, shiny patch of tough new scar.
Figure 2.1b-II The stages of secondary wound healing (healing by second intention)
In general, secondary wound healing is more likely to become problematic than primary wound healing. This is because, in the former, the area of exposed wound is larger, and the new delicate granulation tissue is therefore more likely to become damaged or infected.
There are a number of factors that can negatively affect the healthy course of wound healing. These include the state of nutrition of the body, the richness of the blood supply to the damaged tissue, the presence of infectious organisms or foreign bodies in the wound, and the age of the person.
In malnutrition the response of both the immune system and tissue healing is less efficient. Scurvy, the disease resulting from vitamin C deficiency, is particularly associated with poor wound healing.
In old age, the connective tissue supporting the skin is less vital and more easily damaged, and the healing response is less rapid. A compromised blood supply, such as occurs in the degenerative condition of arteriosclerosis, will also reduce the speed and effectiveness of healing, as this will impair the delivery of the blood that is the source of nutrients and immune cells to the tissues.
Diabetes mellitus is another condition in which the blood supply to the tissues may be compromised. The nerve supply to the tissues may be deficient, meaning that injuries are more easily sustained, and there is an increased risk of minor infections taking hold – this means that wound healing can be very problematic.
Finally, a wound may not heal if it becomes infected or if it becomes repeatedly damaged. This is why such careful attention is given to the application of sterile, strong and breathable dressings in the surgical management of wounds.
Chronic skin ulcer
If a patient has a condition that leads to impaired wound healing, a wound may reach a state of becoming resistant to becoming fully healed. This is particularly likely if it is secondary rather than primary wound healing that is taking place. In such patients, the granulation tissue can easily become infected or damaged, and the wound repeatedly oozes or bleeds. This prevents new skin from growing to close the gap. Such a condition is known as a chronic skin ulcer.
The term chronic refers to the fact that a condition is long-standing. The opposite of the term chronic is acute, meaning short-lived. Contrary to popular understanding, the medical use of these terms does not tell us anything about the severity of a condition. A minor condition can be chronic (e.g. athlete’s foot) and a life-threatening condition can be acute (e.g. heart attack).
A chronic skin ulcer is a condition that can be a cause of great disability as a continually discharging wound is both exhausting and painful. Ulcers also carry a long-term risk as a focus for infectious organisms, and for this reason may result in the need for amputation. Patients with diabetes, poor circulation, immobility or malnutrition are particularly at risk of developing a chronic ulcer. The lower legs and areas in which there is repeated damage (e.g. the feet) or pressure (e.g. the buttocks) are the most common sites for ulcers to develop.
In some people, scars can heal in an abnormal way, with an excessive production of fibrous tissue. This poorly understood condition leads to raised lumps of scar tissue at the site of even minor wounds. These overgrown areas of scarring are known as keloid scars. These can be a cause of distress for the patient, because they may be cosmetically unsightly. Keloid formation appears to be more common in certain individuals and, in particular, in black skin.
Keloid scars are considered very difficult to treat, as simple surgical removal may lead to a scar that produces another keloid. Injection of a corticosteroid preparation into the scar may reduce the swelling in some people.
Conventional treatment of wounds
There are some basic principles that are conventionally followed to enable wounds to heal. These include:
•preventing infection by removing any foreign matter or dead or dying tissue
•encouraging primary wound healing if possible by opposing and stitching the sides of a clean wound
•protecting the healing area with a sterile, breathable, dry dressing
•treating any infection rapidly by cleaning and the use of antibiotics, which are either applied to the wound or taken orally.
Prevention and treatment of poor wound healing and ulcers
In general, there are four broad approaches to someone who is at risk of poor wound healing:
•Preventing injury, for example, attentiveness to skin care in diabetes, and prevention of falls in elderly people.
•Treating the underlying cause, for example, vitamin supplements and increased carbohydrates and proteins in the diet in malnutrition, and improvement of blood supply by means of vascular surgery or drugs that affect the circulation.
•A chronic ulcer requires regular sterile dressing and cleansing of the open wound area. There can be increasing problems with recurrent infection as the bacteria become resistant to the repeated use of antibiotics. Methicillin-resistant Staphylococcus aureus (MRSA) has become a particular problem in chronic wounds in recent years, as this form of the normally harmless skin bacterium is now resistant to all the common antibiotics, and can become a life-threatening condition in the immunocompromised. Ideally, the patient should be under the care of a specialist nursing team – access to expertise in approaches to the healing of ulcers is necessary for complex cases.
Information box 2.1b-I
Wound healing: comments from a Chinese medicine perspective
The Chinese medicine view is that a wound, by disruption of Qi and Blood flow in local Channels, causes impaired flow of Qi and Blood, and thus local Qi and Blood Stagnation. The pain and formation of the blood clot are physical reflections of this. However, here is an example of when Qi and Blood Stagnation in the Channels perhaps may not necessarily signify a wholly negative energetic state, because in this case, from a conventional perspective, the pain and blood clot are both essential to help the healing process.
The intricate processes of healthy wound healing may be seen as manifestations of strong Upright Qi and Blood, and these permit a return to normal flow of the Vital Substances. In particular, the health of the three Chinese Organs of the Spleen and Lung, which govern the muscles and flesh and the transportation of essence to the skin respectively, and of the Kidney, which is the basis of the Yang functions of the Spleen and also supports the grasping of Lung Qi, will be important foundations for wound healing.3
An area of scarring will represent relative Qi and Blood Deficiency in the Channels (indicated by the lack of elasticity and patches of numbness associated with scars), but this will be minimal if healing by first intention is possible. This should make sense from the perspective of Chinese medicine, because if the edges of the wound can be brought together, it will mean that the natural flow of Qi and Blood in the area is less likely to be disrupted.
If the damage to the area is large and the original shape of the tissues cannot be restored, Qi and Blood Stagnation are likely to be prolonged, and long-term Qi and Blood Deficiency in the area more marked. In the case of scars that remain painful, this suggests persisting Qi and Blood Stagnation.4
Wound healing is dependent on healthy tissue with a rich blood supply and an ability to fight infection. This would suggest that any conditions that involve poor wound healing might point to either a local or a general Blood and Qi Deficiency, and also healing could be complicated if Pathogenic Factors such as Heat, Damp or Phlegm are part of the energetic pattern, either generally or locally. An inherited tendency to poor healing or the poor wound healing seen in old age could indicate an underlying Jing (Kidney Essence) Deficiency.
Healing wounds that continue to ooze blood and fluid suggest the presence of local Heat and/or Damp. However, in Western medicine people with local problems such as this often manifest a number of other symptoms such as poor circulation and cold extremities. This might suggest that the poor wound healing is connected with wider systemic problems such as Deficiency of Spleen Qi, and Spleen not Holding Blood. This is particularly the case in a chronic ulcer, in which poor healing of the underlying flesh might well point to the involvement of the Spleen, which is responsible for the tone and quality of flesh in general.
By contrast, the lumpiness of keloid scars might be interpreted as a manifestation of Phlegm. Preventing a keloid from forming with steroid injections could be interpreted as Moving local Stagnation and Phlegm, but this might carry energetic costs as these injections will not be treating the root imbalance. Steroid injections are recognized to cause thinning and weakening of tissues, and so the benefits of local improvements may come at the price of subsequent local damage of Qi and Yin.