Nutrition (10 page)
CAN WE OR CAN’T WE?
Some researchers have challenged whether the standard statement that mammals cannot make glucose from fatty acids is really true. Plants and nematodes (roundworms) have enzymes that can convert fatty acids to dicarboxylic acids via a metabolic pathway called the glyoxylate cycle, so they can be used for gluconeogenesis. Some of the enzymes involved have been found in animal tissues, and genes coding for them have also been found in non-placental mammals such as the platypus and the opossum. It’s also known that fatty acids with an odd number of carbon atoms, and branched chain fatty acids, can be metabolized to yield succinyl-coenzyme A, which can act as a building block for glucose, but this is not thought to occur in significant amounts.
Energy storage: making glycogen from glucose and vice versa
More often than not, your diet provides excess glucose. When you eat large amounts of carbohydrate in excess of your immediate requirements, it is converted in the liver to the starchy storage molecule glycogen. This process, glycogenesis, is triggered by the presence of the hormone insulin, which is released after a carbohydrate-rich meal.
Glycogen is a complex polymer formed from glucose molecules that are chained together. Branching occurs every ten or so glucose units along the chains, and the whole is wrapped up by a protein, glycogenin, to form a spherical ‘blob’ inside muscle and liver cells. Glucose is easily snipped off the end of the numerous branches whenever it is needed.
Energy storage: making fat from glucose
As little carbohydrate can be stored as glycogen, excess glucose is converted into fatty acids for storage. This process occurs mainly in the liver cells (hepatocytes) and fat cells (adipocytes). Following pregnancy, it also occurs in breast cells during lactation.
During times of excess, plenty of glucose enters the glycolysis pathway within liver and fat cells. Each molecule of glucose produces two molecules of pyruvate, which enter the cell’s mitochondria and are converted to acetyl-coenzyme A as usual. Acetyl-coenzyme A feeds into the first part of the citric acid cycle by combining with oxaloacetate to make citrate. This is the stage at which the cell has to decide whether to continue processing it through the citric acid cycle as usual, to produce energy, or whether to divert it for a rainy day and store it as fat. This decision is an easy one for the cell to make. When carbohydrate is plentiful, the mitochondria are already working at full capacity to produce energy and citrate levels build up, forming a bottleneck in the metabolic pathway. To stop everything clogging up, a control mechanism quickly removes the excess citrate back out of the mitochondria into the main part of the fat cell again. Here, something amazing happens. Increased citrate levels cause the enzymes that promote fatty-acid synthesis to join together, with the vitamin biotin, to form filaments. These filaments act just like factory conveyor belts, converting citrate back into acetyl-coenzyme A and joining them together to form fatty-acid chains of various lengths. It has been calculated that a single liver cell can develop as many as 50,000 of these fatty-acid producing filaments at any one time, if needed.
Once formed, the fatty-acid chains are further processed into triglycerides (made up of glycerol plus three fatty acids). In adipose (fat) cells they are stored as a large droplet of fat in the centre of the cell and you gain weight – sometimes at an alarming rate! Fatty acids formed inside liver cells are not usually kept in the liver. They are packaged with protein, to make them soluble, and sent out into the circulation as particles called very low-density lipoprotein (VLDL). Some triglycerides are also obtained from the diet, and are absorbed from the gut (chylomicrons) for transport to fat cells if they are not needed immediately as a fuel. High levels of circulating VLDL and triglycerides can occur on a high-carbohydrate diet and are associated with an increased risk of hardening and furring-up of the arteries, coronary heart disease and stroke.
Although dietary fats are traditionally blamed for raising blood fat levels, it is mainly a high-carbohydrate diet that causes blood triglycerides to rise (in the process described above) in an undesirable way.
FATTY LIVER
If liver cells are hard-pushed from processing lots of carbohydrates, or alcohol, they start to accumulate fat and the liver undergoes fatty change. This is identical to the process involved in the production of pâté de foie gras from force-fed geese and ducks in Perigord, France. Non-alcoholic fatty liver disease (NAFLD) is becoming an increasingly recognized health problem. Some estimates suggest that it affects as many as one in five people, although many cases are mild and remain undiagnosed. It is most common in people who are obese, have Type 2 diabetes or raised triglyceride levels. In some cases, it can progress to cause liver inflammation and scarring.
Vitamins play a fundamental role in keeping your body’s metabolic reactions running smoothly and efficiently. When one or more of these micronutrients are lacking, metabolic reactions may slow down or even fail, so your cells cannot function properly. Despite their importance, most of these micronutrients cannot be made in the body and so must come from your diet. The few that can be made (niacin, vitamin D) are rarely produced in sufficient amounts to meet your needs, and are also classed as ‘essential’.
Although vitamins are necessary for health, you only need to obtain tiny amounts from your food. The quantities needed are measured in milligrams (mg) or micrograms (mcg).
VITAMIN UNITS
1 milligram = one thousandth of a gram (1/1,000 or 10
−3
grams)
−3
grams)
1 microgram = one millionth of a gram (1/1,000,000 or 10
−6
grams)
−6
grams)
1 milligram therefore = 1,000 micrograms.
How do you know how much you need?
Everyone has different, individual needs for each vitamin and mineral, depending on their age, weight, level of activity and the metabolic pathways and enzyme systems they have inherited. Some people need more vitamins and minerals, while some need fewer.
The requirement for each nutrient is therefore calculated according to the best available assessment of average needs. These are calculated using volunteers who undergo a variety of laboratory tests to determine how much of a particular nutrient is needed to maintain a certain blood level or tissue concentration, or how much can prevent signs of deficiency disease.
Different countries take a different approach to setting their recommended daily amounts. One way, used in the UK, is to take the estimated average requirement (EAR) for a particular nutrient and perform some clever number-crunching. First, the statisticians assume that the different needs of everyone in the population form what is known as a normal distribution, with a bell-shaped curve spread on either side of the average. From this distribution, statisticians then work out the standard deviation – a measure of how widely the needs of each individual in the studied population is spread away from the average. A range is then created by taking a value that is two standard deviations on either side of the EAR. This produces a range of intakes that, statistically, encompasses the needs of 95 per cent of the population.
The bottom end of the range (i.e. two standard deviations below the estimated average requirement) is set as the lower-reference nutrient intake (LRNI). Statistically, 2.5 per cent of the studied population will have a low need that is met by this intake, but for 97.5 per cent of the population, this level of intake is inadequate.
The upper level of the range (i.e. two standard deviations above the estimated average intake) is set as the reference nutrient intake (RNI). Statistically, 2.5 per cent of the studied population will have a higher need that is not met by this intake, but for 97.5 per cent of the population, this level of intake is sufficient. This level is therefore set as the reference nutrient intake or recommended daily amount.
You may ask why the reference nutrient intake (RNI) is knowingly set so that it will not meet the needs of 2.5 per cent of the population. A good question! Essentially it’s because some nutrients may cause toxicity problems for some people – especially those whose needs fall below the LRNI.
A note about deficiencies
In an ideal world, you would get all the vitamins, minerals and essential fatty acids you need from your food. However, we live in the real world where the average adult fails to eat the minimum recommendation of five portions a day of fruit and vegetables, and seven out of ten adults eat no oily fish at all. Even when we do eat reasonable amounts of healthy foods, their nutritional content is often reduced compared with just a generation ago due to being harvested when unripe, then flown to another country and ripened away from its nutrient-absorbing roots.
As a result of poor food choices (cheap processed foods, take-aways) as well as cutting back to lose weight, a surprising number of people are lacking in important vitamins and minerals. This is not always obvious from national assessments of average food intakes because an average is only an average – some will obtain more, while a significant number are getting less. For example, the most recent National Diet and Nutrition Survey in the UK (2010) suggests that most people are meeting the reference nutrient intake (RNI), or are close to it.
Happy days? Sadly not. These averages hide the fact that a substantial number of adults have intakes that are less than the lower-reference nutrient intake (LRNI). Although 2.5 per cent of people do need intakes that are less than the LRNI, sadly it is usually people with higher needs (especially the elderly) who obtain these lower amounts.
Many doctors and dieticians claim that micronutrient deficiencies are rare in the developed world. Unfortunately, this is not the case, as the National Diet and Nutrition Survey for 2010 showed. It found that nine out of ten women and eight out of ten children do not obtain recommended amounts of iron; that more than a third of women do not get enough vitamin A, calcium, magnesium, zinc, copper or iodine; that half of men have low intakes of vitamin A and that more than 40 per cent do not obtain enough zinc or magnesium; that 97 per cent of older people do not obtain adequate intakes of nutrients that are vital for good health; that one in four adults have blood levels of vitamin D that are too low for normal bone health. In fact, one in five children in a Southampton study (32 per cent) had vitamin D insufficiency and 8 per cent had overt vitamin D deficiency with bone signs associated with rickets.
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