Time to refuel? (Or not!)
One of man’s clever inventions is the fuel gauge used in cars. In modern ones, there is often even a warning light that comes on when it’s ‘time to refuel’. Another is the valve on fuel-filling nozzles that shuts off to prevent overfilling and wastage/spilling. But our human body has analogous devices, too.
Humans need to refuel, too
Once, while lunching with an older acquaintance, I complimented him on his slim physique at a time when many in society were tending towards obesity. His answer astonished me. He said, “I can’t take any credit for that because it seems I don’t have the urge to eat that other folks have.” He could not recall ever having known what it was like to feel ‘hungry’. Eating gave him no pleasure nor was there any urge to do so. “The only reason I know I have to eat is because experience has shown that if I don’t, after a day or so I notice I’m tired and listless. So I know I have to eat to get my energy back.”
It seems his internal ‘fuel gauge’ and ‘low-fuel warning light’ were broken.
‘Enough fuel, already!’
Our body also has an appetite ‘switch-off’ mechanism similar in effect to the automatic cut-off of a fuel nozzle, so as not to ‘over-fill’. In some obese people the ‘Enough fuel, already!’ click-off mechanism is known to be faulty. However, it can be hard to identify precisely where the problem lies, as a range of hormones is known to be involved in the body’s food-feedback systems, and the processes are far from fully understood. However, some insights are emerging.
The leptin hormone
In the 1990s, scientists discovered the hormone leptin, produced by the ob gene.1 Leptin is now known to curb appetite.2 High levels activate certain of the brain’s nerve cells, or neurons, in a way that suppresses the desire to eat, instead generating a feeling of ‘fullness’. Low levels, on the other hand, stimulate hunger.
How exactly leptin achieves this, and thus helps the body’s delicate balance between energy intake (eating) and energy usage (exercise and metabolism), isn’t completely known yet. Many scientists suspect that leptin might be as crucial as the hormone insulin in this function. When leptin levels are low, the sight and smell of tasty food can stimulate an immediate desire to eat. But sight and smell don’t have anything like the same impact when leptin levels are high.
Researchers have observed that giving the leptin hormone to obese people born without the ob gene (and who thus lacked their own naturally-produced leptin) reduced their hunger pangs. They ate less, and so were able to lose weight.
Unfortunately for those who might therefore have hoped that leptin could be used to treat all obesity, “the story turned out to be much more complicated”.2 It’s only a minority of obese people who lack the ob gene. Most obese people have the ob gene, but it produces so much leptin that they’ve become resistant to its effects. Researchers are endeavouring to understand the mechanism of that resistance.3
The ghrelin hormone
Another hormone now known to have a key role in appetite is ghrelin, which stimulates appetite. As the stomach empties itself of the previous meal, bloodstream levels of the ghrelin hormone rise rapidly, signalling to the body that “it’s time to eat!” Then as soon as the stomach becomes full, ghrelin levels fall again.
In people who lose weight through dieting, ghrelin levels become “chronically high”—which might help explain why many people struggle to adhere to such weight loss programs.2
The melanocortin–4 receptors
Researchers are also investigating the receptors, or ‘docking sites’, on neurons for a hormone called
When these receptors are working properly, they help to suppress appetite. But defective receptors lead to “morbid obesity”.2
These hard-won insights into the intricacies of the body’s appetite-control systems point to far greater complexity than that of the car fuel gauge and nozzle overfill-prevention mechanisms. Surely nobody would say that fuel gauges and automatic pump shut-off gadgetry were not designed. The human engineers certainly deserve the credit for their designs, so how much more honour is due to the Designer of the human body’s intricate stomach-sight-smell intertwined feedback systems? And the fact that they now don’t always work is the result of Adam’s fall into sin, which brought about God’s just curse on creation (see also box below).4
When someone is born lacking hunger signals, or with the defective food-feedback mechanisms in certain obese people today, these are examples of genomic decay (mutations). This is all part of the “bondage to decay” (Romans 8:19–22) to which the originally “very good” creation (Genesis 1:31) was subjected—because of the first man’s sin (Genesis 2:16–17, 3; Romans 5:12,17; 1 Corinthians 15:21–22). No wonder then that genomic decay (due to mutations) is increasingly in evidence.5 E.g. people lacking the ob gene, or unresponsive to the appetite-suppressing leptin it produces, or with defective melanocortin–4 receptors.6
References and notes
- Zhang, Y., and 6 others, Positional cloning of the mouse obese gene and its human homologue, Nature 372(6505):425–432, 1994. Return to text.
- Society for Neuroscience, Brain briefings—Appetite and food intake, sfn.org, November 2007. Return to text.
- Like Type 2 diabetes and other modern ‘scourges’, it may be related to the increasing shift to high energy density and high-glycemic-index refined grains and sugars and away from fruit and vegetables, especially in developed countries. Return to text.
- Smith, H., Cosmic and universal death from. Adam’s Fall: an exegesis of Romans 8:19–23, J. Creation 21(1):75–85, 2007; creation.com/ romans8. Return to text.
- Catchpoole, D., Time—no friend of evolution, Creation 34(3):30–31, 2012; creation.com/time-genetic. Return to text.
- Interestingly, estrogen has been found to use the same pathways as leptin uses to suppress appetite—“a possible reason why women tend to gain weight after menopause.” (see main text, ref. 2) Return to text.