Obesity and food – accumulation of the unused: Part III (Inherent limitations of metabolism and poor obesity control)

Obesity and food – accumulation of the unused: Part III (Inherent limitations of metabolism and poor obesity control)

(Not surprisingly, sophisticated controls are built into our diet intake and metabolism of its products to rein in unbridled obesity. But various factors – some of them autonomous – can override and nullify these controls. Even if you find the details intricate, do grasp that continuously controlling what you can, can be life-saving as we will see in the next post).

It may sound laughable that there could be any intricacy in feeling hungry and stopping eating when satiated. What is less laughable is that the macronutrients in our diet – carbs, proteins and oils/fats – trigger varying, somewhat flawed controls on their own intakes with alarming results. What is the least laughable is that oils/fats bribe their way into our body (greasing palms!), tend to get stored (obesity) and are difficult to dislodge thru simple physical exercise. Haven’t you seen helplessly fat people?

The intricate control of nutrient intake and its flaws

Intake control: Hypothalamus – a part of the brain – is the ‘nerve center’ (along with other factors like blood glucose level) that makes you feel hungry or ‘full’ in terms of food intake. But within this ‘gross’ control, there are intricate controls at play that control individual nutrient inputs, principally carbohydrates, fats and proteins, and help control obesity. As a corollary, flaws in this mechanism is the primary reason for obesity.

Energy balance as a control mechanism: We know from the previous post that glucose, amino acids and fatty acids have ‘potential chemical energy’ which is unleashed during metabolism – mostly to release energy for work (and workouts) and body temperature maintenance and for tissue building and repair and chemical synthesis. Our long term energy balance is the balance of input over its disappearance by oxidation and energy release, over a period of time. (refer previous post OBESITY AND FOOD – ACCUMULATION OF THE UNUSED: PART II (DETAILS OF HOW THE FOOD-OBESITY LINKAGE PLAYS OUT) for ‘metabolism’). Obviously, the input must be and is controlled by the balance i.e. the input (or intake) must reduce in the face of large balance and vice versa.

Flaws in energy balance-led controls: It is believed that inherently low metabolic rate (i.e. slow utilization of nutrients leading to sustained high levels in the blood leading to forced storage), low exercise levels (i.e. limited consumption by oxidation for energy release) and some socio-economic factors, individually as well as in combination, can disturb this in-built control mechanism leading to food intake in excess of requirement. Oxidization of fats (or oils) is inherently slow and inefficient given their complex molecular structure (refer Post 17, EDIBLE OILS: AN INTRODUCTION – THE MULTI-FACETED PERSONALITY OF OUR COOKING OILS) and without rigorous aerobic activity, lag in consumption leading to storage possibilities. Moreover, the satiety signals from fat consumption are weak causing some uncontrolled consumption.

Glucose, the dominant routine energy source: We know that glucose is the most preferred energy source (and brain’s favorite) followed by fats and amino acids but that only means that their consumption rates are vastly different; they are still consumed simultaneously. Amino acids are rarely pulled into oxidation for energy; their primary role is building and repair of tissue (prominent in young, growing bodies) and synthesis of enzymes, hormones and neuro-transmitters but it is still metabolism of the ‘building type’.  Average protein requirement of a typical adult Indian is about 60 g/day and comes from milk, lentils (daals), legumes or beans or kathol and wheat in case of vegetarians. These foods bring in more carbohydrates than proteins which is consistent with a lot larger energy requirement than growth requirement.

Thus, the main energy suppliers are carbohydrates (starch and sugar) and oils/fats which oxidize at different rates. During a typical day, carbohydrates are a lot more likely to be consumed completely than fats which, in case of generous intake, can accumulate.

Blood glucose levels thru the night: It has been shown that glucose and amino acid metabolism rate is normally stimulated by intake to limit the blood levels (or ‘concentration’). This ties with the fundamental law of reaction rates that ‘higher concentration promotes higher reaction rate’. Mornings present an interesting challenge. The high chemical potential available after dinner has slowly (because of low metabolic rate) decreased over last 12 hours in absence of any input and led to a low residual level in the morning (for non-diabetics) which was tolerated because of inactivity. (Typical ‘fasting blood glucose level’ in non-diabetic adults: about 100 mg/dL).  But increasing activity level in the morning (with more to follow) at low availability level cries out for replenishment.  ‘Breakfast like a king’ must have stemmed from this.

It is for this reason that a cup of hot milk at bedtime is sometimes recommended to people with fast metabolism; very low blood glucose level at, say, 3 am can disturb sleep. Midnight fridge raids are a strict no-no for all because input in absence of consumption is bound to lead to accumulation, even if digestion holds out!

Daytime blood glucose levels: Two hours after lunch, i.e. in the middle of injection of digested nutrients into blood stream, day-time metabolism quickly eats up glucose to typically bring it to 120 mg/dL (‘post-prandial’), in non–diabetics. Note the relatively small distance from ‘fasting sugar’, as a result of active metabolism. As it tapers off towards the evening due to steady activity, the low blood level makes you long for dinner (sometimes pushing you to an evening snack!). Afternoon tea – especially the English type! – probably originated from this.

The problematic control of fat metabolism and obesity development: Fat oxidation (sometimes already hereditarily compromised) is intrinsically slow and is driven passively by the difference between total energy requirement and energy available from glucose (and to some extent, amino acids) metabolism. It also has a weak relationship with its own intake unlike proteins and carbohydrates. Thus fat oxidation picks up only when energy requirement is high (as in sustained aerobic exercise) and the energy available from others is low. Thus a good food intake (meaning enough of all three macronutrients) without sustained physical activity will not stimulate fat oxidation forcing them to be stored. To compound the matters, fat intake-induced satiety is also weak.

Thus we can list the following reasons for obesity development:

  1. Weak satiety signals from fat/oil intake, their inefficient and sluggish oxidation for energy release and relatively weak intake control. Worryingly, it has been found that obese subjects instinctively reach out for high fat foods from a large spread. A classical case of a bad thing being attractive!
  2. Quick and efficient glucose oxidation for moderate activity sparing fats. Proteins are different.
  3. Lack of physical activity not summoning fats for energy release which are slow releasers anyway.

Interestingly, while the fat intake per se’ has been the proven culprit, it has been difficult to conclude how the nature of fat (saturated or unsaturated) influences obesity except in where it ends up in the bodily adipose tissue. Of course, the unsaturated fats remain possible routes to introduction of ‘oxidized molecules and free radicals’ into the blood and following pathogenesis. (Refer Post 16, OXYGEN, FOOD AND LIFE : PART II (THE DARK SIDE OF OXYGEN). (Interestingly, stearic acid – the most abundant fatty acid which imparts saturated character to oils and fats – has now been absolved of tendency to raise blood cholesterol levels.)

A review of nutrient metabolism:

  1. Glucose, fatty acids and amino acids as potential energy carriers: These are store-houses of chemical potential energy by virtue of their molecular structure i.e. the chemical bonds in them release energy when broken by oxidation and get converted to low-energy water and carbon dioxide.
  2. Glucose – the most efficient and ‘popular’ energy source: Of these, glucose is the most efficient in terms of the speed at which it reacts with oxygen (or ‘burns’) to release energy and its oxygen requirement. Brain is particularly partial to glucose as energy source, yawning at the end of a strenuous brain exercise is a sign of brain crying out for a glucose shot. ‘Glucose saline’ is the basic intravenous, life-sustaining drip to bed-ridden patients whose dietary inputs are impaired. Carrying a few sugar candies in your pocket during a three hour strenuous exam and not skipping a light breakfast before it is a good idea.
  3. Intermediate energy carriers: All three macro- or bulk nutrients end up as carbon dioxide and water having ‘invested’ the released energy into molecules called Adinosine triphosphate (ATP) and Creatine phosphate (CP) – mainly the former. It is these two that gradually release energy for work. This efficiently ‘spreads out in time’ energy availability quickly introduced by food and converted by metabolism.
  4. Changing blood glucose level: Blood glucose level dips as it is consumed for work. The ‘fasting serum glucose level’ – typically less than 100 mg/dL in adult non-diabetics – is the residual glucose level in the morning after all the slowed consumption after dinner the previous evening. If low daytime physical activity and/or excessive carbohydrate intake have tended to keep it high, it is converted to a starch-like, insoluble bio-polymer called glycogen and stored in the liver and voluntary muscles.
  5. Limited glycogen storage capacity: However, body’s glycogen storage capacity is limited – a maximum of only about 2000 calories at a time. This is an average adult’s daily requirement with routine activities. In absence of dietary replenishment, all the glycogen in the body would be exhausted at day’s end even without rigorous activity.
  6. How glycogen is released and used: As physical activity starts, the skeletal or voluntary muscles start eating up glucose from their blood supply. Soon, their own glycogen starts breaking down into glucose which directly releases energy for exertion. This obviously happens only if physical activity is sustained.
  7. Fat enters the energy fray when the demand is large and insistent: For circulating fat to be combusted for energy release at a significant rate, low available glucose level – which automatically means reduced carbohydrate intake and sustained aerobic activity reducing circulating glucose as well as glycogen-origin glucose. For slimming (weight reduction because of reduction in physical storage), physical activity has to continue and energy input controlled.

This, then, is a detailed account of what obesity is, how it is a result of several dynamic physiological phenomena, how some factors or reasons cannot be controlled and what can be done within our control to arrest its growth. Given its complexity, we have decided to devote one last post as a ‘synopsis’ of obesity focusing what can be done practically to reduce it.

Next Post:

Obesity and food – accumulation of the unused: Part IV

Let’s control what we can without fretting about what we can’t

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