Comment on “Kids’ Sugar Cravings Might Be Biological” on Morning Edition Sept 26, 2011 where it was reported that sugar cravings are not an indicator of tendency toward obesity, but are found naturally in all children. Thus controlling obesity in children will not be successful if the only method used is an attempt to change the motivation of children toward sweets. The report relates sweetness preference instead to pain relief and to helping to promote growth in height.
NPR reporter Gretchen Cuda Kroen highlighted two research studies on sugar preferences in children by interviewing Julie Mennella of the Monel Chemical Senses Center and Susan E. Coldwell of the University of Washington, Seattle. Both studied sweetness preferences in children, looking for reasons why children preferred higher sweetness, but from two different angles. Pepino and Mennella (2005) compared the child’s (aged 5-10 yr) with its mother’s preferences (same genes and environment, average age 35.4 yr) and the ability of sugar to reduce pain sensitivity.
Coldwell et al (2009) studied the changes in sweetness preference in adolescents undergoing puberty changes in varying degrees (with sample participants from pre-pubescence, some from post-pubescence, and some from in between). Cuda Kroen uses the term “hardwired” to describe the fact that infants are born with a preference for sugar from “day one”. Pepino and Mennella (2005) also point out that children are sensitive to bitterness, too (explaining the resistance toward eating vegetables, which NPR reported last year could also be due to physiological differences in being able to taste the bitterness).
The report concentrated on the finding by Coldwell et al (2009) that supported previous research suggesting an upper age limit for this “super-sized sugar preference.” Coldwell et al (2009) found that the loss in sugar preference seemed to coincide most strongly with the drop in a marker of bone growth in the urine. They conclude that sweetness preference loss tracks more closely with a slowing of growth than with hormones most commonly associated with puberty.
My Comment Posted at NPR
What do you mean “might be biological?” As opposed to What? There is no way they can get cravings unless it is “biological”. I hate the use of this term to imply that on the one hand, there is biology, and on the other hand, …what? If they want to imply genetic control, then use that term. However, genes do not cause any difference seen in people. It is the interaction between genes and environment that results in what has been attributed to “genetic difference”. If people’s physiology is different, then say that differences in physiology seem to be involved. Physiological differences are often due to acquired differences in what is present inside the body, e.g. situations that the body must handle differently from another person.
From the neuroscientific evidence on taste buds (Chaudhari et al 2010, Bradbury 2004), we need to realize that taste is a factor in helping to regulate body metabolism but is not in any way a sole predictor of body weight changes. The report emphasizes that we cannot assume that preference for sugar is something bad in children. More importantly, this study shows that we have to realize that our overweight population of children is probably due to multiple causes, and not just to overeating. The “calories in = calories out” model is clearly a HUGE oversimplification. The study reported here is just one of many that have attempted to get at what happens at the “=” sign in the above equation. (see my blog post “Sweetness Preferences Change at Puberty” at https://marthalhyde.wordpress.com/2011/09/30/sweetness-preferences-change-at-puberty/ for more discussion about what taste receptors are for, how they work, and problems with many scientific explanations.)
More of My Ideas
Scientific Method and “Genetics” as Explanation
“Genetic differences” may actually be physiological differences, explained by the presence of toxins or other traumatic assaults that force the nervous system to write alternative programs as workarounds–something that any body of any genetic background would do. If there are differences in genes, these could also have been acquired, as in mutations caused by certain toxins present in the tissues where these genes are being expressed. We have to be careful about our conclusions because, even if genetic differences are found that are associated with a difference in physiology, we must always ask first, are these genes found in the eggs of the mother and/or sperm of the father? Did the sample of tissue from the person being genetically analyzed come from only those places most likely to be exposed to mutagenic toxins? or were there multiple samples taken from all over the body, from deep inside organs not likely to be exposed to the toxin and analyzed separately?
If all samples are pooled together and genetically analyzed, then we still do not know if the genetic difference was acquired during life or passed down from the parent, or if the parent had acquired it via exposure to mutagenic toxins–a high likelihood, since toxins will pool in the body’s lower regions–groin, pelvic cavity, hands and feet. We have to conclude that this simplistic attitude toward genetic information is incredibly misleading. Precision is important because its lack has caused both news reporters and physicians to say there are genetic differences in particular characteristics where there are no genes even recognized as being associated with that characteristic. Because of this misunderstanding, the recommended action by a patient with a characteristic is often misapplied.
What Taste Tells Us
There is no way that bone directly tells the tongue anything, since there is no direct innervation between the two. Anything bone secretes into the blood will go to the brain first. However, this news report points to a couple of articles that show that bone appears to talk with fat cells and with the pancreas to coordinate metabolism with bone growth. Taste buds are the brain’s way to detect the chemistry of the food going into the body, providing information to the brain that can be used to alter the pancreatic responses to the bone-fat conversation.
There is strong evidence (Bradbury 2004) to suggest that sweet receptors tell the brain of the easily digestible carbohydrate level of the food. Due to the nature of sour receptors, the body can only tell the brain about the acidity of the food when ions like chlorine and bromine are present. Salt receptors tell us the presence of different kinds of salts, no doubt the ratio of two chemical elements, chlorine to a basic ion, such as sodium, magnesium or calcium, since the ratio is more important to the brain than the fact that a salt is present.
Bitter receptors tell us what is possibly poisonous to us and, more specifically, if there is too much of one of 3 chemical elements (arsenic, manganese, potassium) or several amino acids that give that bitter taste to our food: . We obviously need manganese and potassium, but not in extremely high amounts. Bananas have a lot of sugar in them, but plantains do not. Both have lots of potassium, but plantains can be obviously bitter in taste. However, bananas can have a slightly bitter aftertaste attributable to the potassium. Both chocolate and coffee can be bitter, due to the high amounts of manganese in them.
Arsenic is clearly poisonous to us but, like potassium, must be present in fairly high amounts to kill us. Because of this property, it is the poison of choice for those who want to hide the fact they are poisoning a person. However, arsenic at any dose does harm us. It can accumulate in certain tissues of the body. It interferes with the activity of boron everywhere it is found. Boron is a chemical element necessary for connective tissue repair and maintenance, especially that of the heart. The heart has the greatest need for constant repair and maintenance when compared with tendons, ligaments, bone, and other collagenous tissues of the body. Thus, arsenic poisoning is often found when there are unexplained heart problems. A patient practicing mindfulness techniques would probably become aware of connective tissue failures that would raise an alarm to check for arsenic long before cardiac issues arise.
Finally, umami receptors tell us protein content of our food, because they sense the presence of amino acids. We can conclude from these observations that taste receptors perform a fairly complex role in telling the brain about the content of our food.
“Genetics” vs “Hardwired”
So what does “hardwired” mean? To many people, the word “genetics” comes to mind, but we do not have to invoke that hand-waving term to understand how preference for sugar is so engrained in us at an early age. Brain circuits using the information from taste buds can be an almost inevitable outcome of simple developmental programs that depend upon environmental input to be written into our brains, an environment that is so carefully controlled in mammals that development in us becomes predictably consistent among babies. The only clear differences that most would agree are obviously non-genetically caused are the developmental defects that appear because of a known toxin, such as cocaine. However, even so-called genetic defects may be caused by toxins that were not caught by doctors.
Because some toxins are mutagenic, their effect may even be seen in families without being passed down from generation to generation. How? Most Americans tend to live near their relatives, not moving far from the place of birth. Genetic population analysis shows this to be the case. We do not see the other extreme. I know of no family where both parents raise their kids in one house, and then both parents drive to another house that is in a very different neighborhood to sleep at night. Divorce generally moves only one parent away from the kids. A very important control in this “genetic experiment”, therefore, is lacking. We have to realize that conclusions about genetic background remain very questionable, except for the most extreme examples.
So what appears to be “hard-wired” is probably mostly due to the programs that get put into place in the developing nervous tissue to deal with the changing internal environment of the developing embryo. One of the developmental programs for handling taste involves the wiring of cranial nerve X to innervate taste buds in the back of the tongue in the infant, through adolescence, adding a third cranial nerve that handles taste at these ages, but which is lost eventually, leaving only two cranial nerves handling taste in the adult.
What is more important for this report is the likelihood that the brain, and not the tongue is more important for this amplified sugar preference. There is a gustatory center in the anterior medulla that amplifies the information coming in from cranial nerves VII and IX from the tongue carrying sweet taste that is most active in the infant and which doesn’t lose its ability to amplify the sweet taste in the brain until puberty in the adult. Given the nature of brain activity, it is more likely to be timing signals sent from the suprachiasmatic nucleus in the hypothalamus and not reproductive hormone levels that trigger the end of this amplification by the gustatory center, since hormone levels at puberty are so unpredictable at that time.
Cause of Change in Sweetness Preferences
This news report asks about the primacy of certain signals for sugar preferences: puberty hormones or growth/metabolism. We know that testosterone causes epiphyses to seal at the ends of long bones, causing bone growth in length to end, and both sexes have increases in testosterone produced at puberty. One important aspect of hormone physiology is that the amount of the hormone change is not nearly as important as the fact that hormone levels do change at all, since exact levels can be maintained so easily through simple feedback mechanisms. So, we can see that a drop in progesterone (some think LH) level can induce menstruation, and any increase in testosterone can induce epiphyses to seal. Not directly measured in this report is the response in bone to increases in testosterone (because its effects are more difficult to measure in bone), but rather a more distant measure of bone turnover rate which correlates with changes in height. It can be readily seen to change with the cessation of increases in bone length.
This news report raises doubts that the obesity problem in our children can be easily managed managing motivation, like teaching our children to choose more healthy alternatives and to avoid the high sugar content of less healthy foods. They aren’t going to choose less sugar if high amounts are available. Motivation will always be slanted toward getting more sugar, not less, and will not change until puberty. The research discussed in this report clearly shows that something about changes in bone growth and metabolism is more important than some of the effects of puberty hormones for determining the change in sugar preference in children. In other words, as long as kids are growing, they will want sugar at the highest concentration they can get, regardless of when puberty starts.
References Cited in This Comment and in NPR Report
Bradbury, Jane. 2004. Taste Perception: Cracking the code. PLoS Biol 2(3): e64
Chaudhari,Nirupa; Roper,Stephen D. 2010. The cell biology of taste. J.Cell Biol. vol. 190 no. 3 285-296.
Coldwell, Susan E.; Oswald, Teresa K.; Reed, Danielle R. 2009. A marker of growth differs between adolescents with high vs. low sugar preference. Physiology & Behavior Volume 96, Issues 4-5, Pages 574-580.
Pepino, M. Yanina; Mennella, Julie A. 2005. Sucrose-induced analgesia is related to sweet preferences in children but not adults. Pain 119(1-3): 210–218.
Lee, Na Kyung; Sowa, Hideaki; Hinoi, Eiichi; Ferron, Mathieu; Ahn, Jong Deok; Confavreux, Cyrille; Dacquin,R omain; Mee, Patrick J.; McKee, Marc D.; Jung, Dae Young; Zhang, Zhiyou; Kim, Jason K.; Mauvais-Jarvis, Franck; Ducy, Patricia; Karsenty, Gerard. 2007. Endocrine regulation of energy metabolism by the skeleton. Cell 130(3): 456-469.
Coombs, Amy. 2007. Endocrine role for skeleton. The Scientist 8 Aug 2007
Ventura, Alison K.; Mennella, Julie A. 2011. Innate and learned preferences for sweet taste during childhood. Current Opinion in Clinical Nutrition & Metabolic Care, 14(4): 379–384.
For other reports on nutrition, see “Nutrition Reviews”
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