An individual whose intake of a nutrient is insufficient for his or her needs is described as suffering from a nutritional deficiency. Deficiencies can be overt or sub-clinical. Overt deficiencies are often given specific names, as follows:
|The anaemias||Nutritional anaemias occur when the oxygen-carrying capacity of the blood is reduced due to a deficiency of one or more of the nutrients required for red blood cell formation. Symptoms of anaemia may include fatigue, breathlessness on exertion, dizziness and pallor.
Iron deficiency anaemia is the most common type of anaemia. Other nutritional anaemias include folic acid, vitamin B2, vitamin B6 (often associated with taking the contraceptive pill), vitamin B12, vitamins C and E, copper, zinc and protein, in which deficiencies of these nutrients result in inadequate red blood cell formation.
Macrocytic anaemia, characterized by reduced numbers of abnormally large, malformed red blood cells, is caused by vitamin B12 and folic acid deficiencies.
Pernicious anaemia, caused by a failure to absorb vitamin B12 (often because of a lack of intrinsic factor) is a type of macrocytic anaemia.
|Beri-beri||A disease resulting from prolonged, severe vitamin B1 (thiamine) deficiency. This disease used to be particularly common in the far east due to the consumption of polished rice. Early signs and symptoms of beri-beri include anorexia, indigestion, constipation, malaise, calf muscle tenderness, palpitations and ‘pins and needles’ in the legs. More advanced cases develop into either of two sets of symptoms, referred to as ‘wet’ or ‘dry’ beri-beri. Wet beri-beri signs and symptoms include oedema, heart insufficiency, digestive disorders, emaciation, tense, painful calf muscles, high blood pressure and decreased urine volume. Dry beri-beri signs and symptoms include memory loss, disorientation and nystagmus.|
|Kwashiorkor||A type of severe protein-energy malnutrition commonly found in the third world, especially in children. The signs and symptoms are oedema, failure to thrive and grow, apathy, impaired mental development, dermatosis, reduced immunity, sparse hair, and vitamin deficiencies (particularly vitamin A).|
|Marasmus||Similar to kwashiorkor, but used to describe protein-energy malnutrition in infants or in children who have adapted to the deficiency by retarded growth, thus avoiding some of the kwashiorkor symptoms. The signs and symptoms are sparse hair, wasting of body fat and muscles with shrunken, wizened appearance, and anaemia.|
|Osteomalacia||Sometimes known as adult rickets, this is a softening of the bones, accompanied by weakness, fracture, pain, anorexia and weight loss, caused by a lack of vitamin D, calcium or phosphorus, leading to problems with bone mineralization.|
|Pellagra||A disease resulting from prolonged, severe vitamin B3 (niacin) deficiency. Pellagra occurred mainly where people used corn as a staple of their diet without processing it with lime (as Mexican people do) to render the niacin bioavailable. Parts of the world where pellagra used to be endemic were Spain, Italy and the southern states of the US. Signs and symptoms of pellagra include muscular weakness, anorexia, indigestion, cracked pigmented scaly dermatitis on parts of the skin exposed to sunlight, tremors, sore red tongue, confusion, disorientation and neuritis.|
|Rickets||A disease of children, associated with malformation of the bones due to dietary vitamin D deficiency or lack of exposure to sunlight (required to allow the body to synthesize its own vitamin D). In rickets the bones are not strong and rigid enough to support body weight and stresses, resulting in knock-knees, bow legs, pigeon breast and skull deformity. In adulthood, softening of the bones due to vitamin D deficiency is known as osteomalacia.|
|Scurvy||Vitamin C deficiency disease. Signs and symptoms include weakness, poor appetite and growth, anaemia, swollen, inflamed gums, loosened teeth, small haemorrhages under the skin and severe infections. Wounds may fail to heal, and scars may break open.|
The effects of nutritional deficiency can be experienced anywhere on a scale from overt deficiency disease to mild hypofunction of the immune, endocrine, nervous or other systems. Commonly used blood tests may fail to identify a problem since the blood is subject to what is known as ‘homoeostatic control’, that is to say blood nutrient levels are always more or less constant. They have to be kept constant because excessive variations could be dangerous. For instance if blood calcium levels are getting low, the body could develop a dangerous condition known as ‘tetany’, leading to convulsions. So the blood borrows calcium from the bones, hoping to put it back later. If the calcium shortage continues, more and more calcium will be ‘borrowed’ from the bones. The blood will continue to show normal calcium readings, but the bones will become demineralized and osteoporotic.
The same applies to most nutrients, and organs or structures other than the bones may be involved. As Adelle Davis, a nutritionist writing in the 1960s remarked:
The first stage of a dietary deficiency occurs when there is failure of supply – either because food is mishandled, the diet is poorly selected, or the individual, for one of many reasons…has increased his needs. Failure of supply may also be initiated or aggravated by difficulties in the digestion, the absorption, or transport of nutrients within the body. Other difficulties may be created by a breakdown in enzyme systems.
Once supply has failed for any of these reasons, there will be a drop in the blood levels of the nutrient. The blood now draws upon the tissues and when that process comes to an end, it borrows from the organ reserves. Note: Although you are well on your way towards trouble at this point, the blood levels of nutrients reveal nothing abnormal, because of the borrowing the body initiates to achieve more equitable distribution of an inadequate supply.
Then functional disability begins – indigestion, nervousness, irritability, a tendency to weep without provocation, a shortening of the memory and attention spans, difficulty in concentration, insomnia, and bad dreams – for which the doctor’s X ray, blood tests, urine analysis, stethoscope and blood-pressure instruments will find no physical justification…
(Eating Right for You, Adelle Davis 1967).
Only if tissue and organ reserves become so depleted that the deficiency begins to show up in the blood, will a condition such as ‘scurvy’ or ‘beri-beri’ be diagnosed. About 30 people a year in Britain die from these diseases, according to a 1991 government survey.
Meanwhile, in people who never reach this drastic endpoint because their deficiency is not absolute, what damage is occurring to their ability to make hormones, corpuscles, enzymes and other substances needed for good health? Drained of the raw materials they need to make these substances, how can the organs function efficiently? Organ biopsies (small samples of tissue) would show a deficiency state more clearly than a blood sample, but would be extremely impractical.
While the initial symptoms of subclinical nutritional deficiency may be minor, such as fatigue, weakness, poor skin condition, lowered immunity, mood changes and other symptoms mentioned above, damage and disturbance to metabolic functions as a result of the deficiency are potentially very serious. For instance a lack of antioxidant nutrients or those needed to metabolize magnesium, methionine or molybdenum may result in an increased level of highly toxic intermediates such as acetaldehyde which are produced by the liver in the course of its detoxification functions. The accumulation of such substances has been linked with the development of diseases such as parkinsonism and motor neurone disease. But because such diseases take many years to develop, no connection with nutritional deficiencies is suspected by conventional medical practitioners.
An inadequate zinc intake can lead to a decreased production of stomach acid and digestive enzymes, and thus ever worsening nutritional deficiencies due to impaired digestion and absorption. Zinc and many other nutrients are needed for countless tasks such as tissue repair, hormone and enzyme production and normal immunity. A very considerable body of scientific literature exists describing beneficial results of studies giving dietary supplements to individuals with a variety of clinical illnesses. Surprisingly, it is sometimes assumed that these positive results have nothing to do with the correction of nutritional deficiency. In fact the nutritional status of the test subjects is often not measured in advance of the studies to ascertain whether there is any difference in results between those with a low or a normal status of the nutrient in question.
It is generally recognized that certain groups of the population are especially vulnerable to develop nutritional deficiencies: pregnant or lactating women, those on weight-loss diets, children and adolescents, and the elderly.
Causes of nutritional deficiency
These can be divided into six main categories:
- Inadequate intake
- Inadequate digestion
- Inadequate absorption
- Inadequate cellular assimilation (absorption into cells and tissues of the body)
- Increased needs
- Increased losses
Causes of inadequate intake
These include poverty, starvation, famine, poor food selection, bad cooking methods, weight-loss diets, ignorance, food fads (particularly in children), dental problems (leading to the selection only of foods which are easy to chew), apathy (particularly in the elderly), anorexia, and a reduced sense of taste. Deficiencies of a number of nutrients such as zinc and B vitamins may lead to anorexia. Zinc deficiency in particular can result in a reduced sense of taste which leads to faddy eating as sufferers unconsciously learn to select only foods with a strong taste such as highly salted or sweetened foods and strong cheese.
Causes of inadequate digestion
These include poor chewing, and a reduced production of gastric acid, bile and pancreatic and gut enzymes. These secretions are in turn dependent on the availability of a number of nutrients such as zinc, amino acids and B vitamins. However protein cannot be broken down to amino acids, nor vitamins and minerals extracted from food without sufficient gastric acid and digestive enzymes.
Causes of inadequate absorption
Nutrients are absorbed through the villi and microvilli located on the walls of the small intestine. The absorption mechanisms may be complex – dependent on carrier molecules which transport the nutrients through the epithelium into the bloodstream on the other side. Other nutrients diffuse through the epithelium.
Nutrients which have not been digested into sufficiently small particles cannot be absorbed through the gut wall. Likewise any inflammation of the gut wall, such as that caused by food allergy, dysbiosis or other sources of irritation, and also increased gut permeability (see Leaky gut syndrome) may cause the gut wall to become dysfunctional and compromise its absorption ability.
Chronic diarrhoea also causes malabsorption, since the contents of the intestine pass through too quickly for proper absorption to take place. Parasitic infestations (e.g. worms) can result in severe malabsorption. In particular tape-worm utilizes vitamin B12, making it unavailable for absorption. Tea, coffee and phytic acid (found in bran) can bind minerals such as zinc and iron in the intestine, making them unavailable for absorption.
Causes of inadequate cellular assimilation
Once nutrients enter the bloodstream, they have to be taken up by the cellular systems which use them. One of the principal problems which can occur with this process is that some toxins commonly present in the body appear to be very similar to essential nutrients. For instance the chemistry of lead resembles calcium so greatly that if calcium is in short supply and there is plenty of lead available, then lead can be absorbed instead of calcium both from the gastrointestinal tract (if ingested) and from the bloodstream into cellular systems.
The problem is that lead cannot perform the same tasks as calcium, so it disrupts the function of the systems which are attempting to use it, and these effectively become calcium-deficient. Countless other toxins can have similar disruptive effects on metabolism and function. They need not be present in large quantities to have these effects.
It is also possible that the mechanisms which pump specific nutrients from the blood into the cells can become damaged by toxins, nutritional deficiencies, or even viruses or other micro-organisms. Symptoms may then occur which suggest that these nutrients are deficient even when large amounts of them are present in the bloodstream. In the illness known as M.E. (myalgic encephalomyelitis) or chronic fatigue syndrome, for example, sufferers have muscle pain thought to be due to chronic muscular spasm, a common symptom of magnesium deficiency. Magnesium supplementation appears to make little difference to sufferers in the short term, but magnesium injections, which flood the cell with very large amounts of magnesium, appear to offer temporary relief. It is thought that in these cases some damage may have occurred to magnesium uptake mechanisms, perhaps by unknown toxins.
The contraceptive pill is one of the many medications which disrupts normal nutrient status in the blood and cells and results in increased requirements. Nutrients most often affected include vitamin B6, folic acid, vitamins C and E and zinc.
When deficiency symptoms seem to occur in the absence of any dietary inadequacy, this is known as a ‘functional’ deficiency. See individual nutrients for deficiency symptoms associated with them.
Causes of increased needs
The ordinary rules of genetic diversity dictate that some individuals will have higher requirements for certain nutrients than others. In addition, smoking, certain medications, heavy exercise, stress, alcohol consumption, pregnancy, breast-feeding, infections and rapid growth are all factors which increase our nutritional requirements.
Experience with the nutritional treatment of many individuals suffering from mental illness suggests that a prolonged nutritional deficiency state can lead to exceptionally raised baseline requirements for certain nutrients, particularly vitamins B3, B6 and zinc. These exceptionally raised requirements have been termed ‘vitamin dependency’ states. Many individuals are not free of symptoms such as hallucinations and severe depression unless these dependency states are acknowledged and appropriately treated. For instance doctors treating pellagra victims in the 1930s observed that some sufferers could only remain symptom-free by taking 600 mg a day of vitamin B3. This is 50 times the amount needed to prevent the disease in those who have never had it. As reported by psychiatrist Dr Abram Hoffer, the treatment of many veterans who suffered arthritis and residual psychiatric symptoms after being detained for lengthy periods in Japanese prisoner-of-war camps in World War II was not fully successful until they were given 1 or more grams a day of vitamin B3.
Causes of increased losses
These include menstruation, heavy prolonged physical work or exercise, diarrhoea, use of diuretics, and hot climates causing heavy sweating.
Laboratory tests for nutritional deficiencies
The measurement of blood levels of nutrients, although widely used in conventional medicine, is not usually sensitive enough to detect sub-clinical deficiencies. Other methods may be more appropriate, depending on the nutrient. Such methods may be ‘functional’ tests, that is to say instead of measuring the nutrient itself, the investigator measures levels of a metabolite (a product of metabolism) which is dependent on the nutrient for its production, before and after supplementation with the nutrient. Low levels of the metabolite before supplementation, followed by significant increases afterwards, can indicate a low ‘activity’ of the nutrient, and therefore a functional deficiency.
|Vitamin A||Vitamin A (retinol) and beta-carotene are usually measured in the serum. Isotope dilution assay with tetradeuterated vitamin A allows the estimation of total body reserves of vitamin A.|
|Vitamin B1||Red blood cell thiamine diphosphate measurements may be more sensitive than the commonly used red blood cell transketolase activity test, since a transketolase effect is sometimes not observed even in severe vitamin B1 deficiency states. Measuring the amount of this vitamin excreted in urine after taking an oral dose of it is also thought to be a reliable method.|
|Vitamin B2||The measurement of the vitamin B2-dependent enzyme glutathione reductase in red blood cells is thought to be the best available method, although several factors such as deficiencies of other nutrients or the age of the red blood cells may interfere with its accuracy.|
|Vitamin B3||Red blood cell NAD levels are thought to be a good indicator of B3 status. The measurement of the two metabolites N-methylnicotinamide and 2-pyr excreted in urine are also thought to be reliable.|
|Vitamin B5||The measurement of coenzyme A activity, which is dependent on pantothenic acid, is thought to be the most reliable indicator.|
|Vitamin B6||Measurement of red cell pyridoxal-5-phosphate (P5P) is thought to be more accurate than plasma pyridoxine. The most reliable functional test is thought to be measurement of the enzyme glutamate amino transferase.|
|Vitamin B12||Elevated urinary methylmalonic acid or homocysteine are indicative of vitamin B12 deficiency. The Schilling test is used to determine vitamin B12 absorption.|
|Biotin||Measurement of the enzyme pyruvate carboxylase in white blood cells before and after treatment of the cell preparation with excess biotin, together with measurement of 3-hydroxy and 2-hydroxyisovaleric acids in the serum.|
|Folic acid||Folate depletion in red blood cells occurs only in the later stages of deficiency, when megaloblastic anaemia may already be present. Microbiological assays (which measure the extent of growth of folate-dependent bacteria cultured with a blood sample) are thought to be more sensitive than red cell levels.|
|Vitamin C||A saturation test may be used to diagnose scurvy: vitamin C is given in multiple small doses. Some hours later vitamin C excretion is measured in the urine. If urinary vitamin levels do not rise, scurvy is present. White cell vitamin C measurements are considered the best available method for assessing vitamin C reserves. Under most circumstances a simple serum vitamin C measurement will suffice.|
|Vitamin D||Measurement of 25-hydroxycholecalciferol in the plasma is thought to be the most reliable method to determine vitamin D reserves.|
|Vitamin E||A useful method to measure vitamin E status is to determine the fragility of red blood cells in the presence of hydrogen peroxide. (Vitamin E deficient red cells burst in the presence of hydrogen peroxide.) Platelet vitamin E levels are thought to be a good method of measuring the dietary intake of vitamin E.|
|Calcium||There is no reliable method for measuring calcium status. Serum calcium is almost always normal. Hair mineral analysis can provide some indication, but high hair calcium levels can reflect a low as well as high calcium status.|
|Chromium||Serum chromium levels are a good indicator of chromium status. Sweat chromium levels correlate well with serum levels. Hair chromium levels can be useful if the hair has received no cosmetic treatments.|
|Copper||Low serum copper levels are rare, even in the presence of deficiency. The measurement of the copper-dependent enzyme superoxide dismutase in red cells is thought to be the best index of copper status.|
|Iron||Measurements of serum ferritin (an iron storage protein) are thought to be a good indicator of iron status. Less expensive is the measurement of serum iron and serum iron-binding capacity (IBC). Low serum iron and high IBC is indicative of iron deficiency.|
|Magnesium||White blood cell magnesium levels are accepted as the definitive test for magnesium status. Measurements of urinary magnesium excretion over a 24-hour period after magnesium loading are also reliable. Red cell magnesium tests are cheaper but their usefulness is limited.|
|Manganese||Serum and sweat manganese levels are considered to be good indicators of manganese status.|
|Phosphorus||Serum inorganic phosphorus and urine phosphate measurements are normally used.|
|Potassium||Red cell potassium is a good indicator of potassium status.|
|Selenium||Levels of the selenium-dependent enzyme glutathione peroxidase in the blood are a sensitive indicator of selenium status. Red cell selenium measurements are also reliable.|
|Sodium||24-hour urinary sodium excretion is a useful indicator. Sodium deficiency is relatively rare.|
|Zinc||White blood cell zinc levels are accepted as the best indicator of zinc status. Sweat zinc levels can be equally sensitive, more so than hair or serum zinc. Also used are the zinc tolerance test, indicating zinc deficiency if plasma zinc does not significantly rise after zinc loading; and the zinc taste test, a fairly crude device in which a 0.1 per cent zinc sulphate solution is given by mouth, suggesting deficiency if the subject cannot taste it.|
|Amino acids||24-hour urinary measurements of amino acids, their metabolites, and the products of the amino acid pathways. Serum levels may also be appropriate.|
|Essential fatty acids (EFAs)||Levels in red cell membranes give a good indication of status. The results should be given as a ‘profile’, which allows imbalances between different fatty acids to be identified. These imbalances can indicate defects in enzymes such as delta-6-desaturase required for EFA metabolism.|