Why are we getting taller as a species?

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IGF-1 insulin-like growth factor 1 is a peptide hormone just like growth hormone, but the two hormones are not the same. Even though there is an observed connection between IGF-1 levels in the blood and the development of certain cancers explained later in the article this fear of IGF-1 in milk is unnecessary.

This could simply be due to the fact, that concentrations of IGF-1 in milk is much lower than the concentrations of IGF-1 in our own digestive fluids present in our gastrointestinal tracts [4]. The amount of IGF-1 in milk is simply too small to have any relevance. As a parent, you might be extra concerned about what your kids gets exposed to, making you consider even minute amounts of hormonal exposure undesirable, and then choosing not to use formula.

That worry is understandable, but there is no reason for it; even though IGF-1 is more resistant to heat treatment than bGH, it is broken down during the special heat treatment that infant formula undergoes [8].

A rise of only 14 micrograms per liter blood [10] which already contains between and micrograms per liter [6] but a rise nevertheless. This kind of rise in the circulating levels of IGF-1 is not a unique consequence of drinking milk. There are lots of foods that boost our own production of IGF An intervention study from showed, that a daily intake of 50 grams of soy protein raised the level of IGF-1 in the blood by 21 micrograms per liter [11].

Since soy contains no IGF-1, the rise must have been due to it being able to boost the pituitary production. Generally it seems that our own production of IGF-1 is dependent on our intake of protein [12]. Whether this comes from animals or plants is irrelevant, and it is reasonable to believe that a low production of IGF-1 is a sign of malnutrition — especially in the elderly [13].

But why are we so concerned about IGF-1 at all? Basic scientific misunderstandings are at the root of most health myths. When it comes to disease, one of the most predominant is, that complex diseases have a single cause. Many believe that diabetes is caused by sugar or even carbohydrate intake, that salt is the cause of high blood pressure, and that IGF-1 causes cancer.

But cancer — as with any of the aforementioned ailments — is a multifactorial disease [14] and any form of cancer is most likely caused by a host of interconnected factors. So when someone claims that one thing — for instance growth hormone or IGF-1 is the cause of cancer — it is always untrue and easy to disprove. What we know is that a high level of circulating IGF-1 might increase the risk of one type of cancer in the prostate — not cancer in general.

That high IGF-1 levels might promote a single type of cancer is a hypothesis, not a fact, and under all circumstances a growth factor as this one would most likely only play a part of an intricate confluence of factors.

Most claims that IGF-1 is the primary cause of any cancer is based on cell studies, which can never be relied upon to establish cause and effect in the complex interactions inside the human body. Cell studies can only give rise to hypotheses or help to explain the mechanisms behind and observed correlation that can be subsequently tested in further scientific studies.

These scientific studies have been done and they show among other things that even when the contents of IGF-1 in the blood is raised a bit, the intake of low fat dairy milk is associated with a lower risk of colorectal cancer — in particular in people with a high level of circulating IGF-1 in the blood [15].

This is the exact opposite result of the hypothesis that milk consumption causes cancer in general and, in the context of the mentioned article, that this process is driven primarily by IGF In the end our primary concern is to know whether certain foods increase the risk of cancer — and not whether certain components of our food does so in isolation or in a petri dish.

Before describing what we actually know about the connection between milk and cancer, we have to first turn our eyes to the last group of milk hormones: A lot of the milk that we drink comes from pregnant cows and as with humans, this means that the levels of circulating estrogens are higher than normal. Since that which happens in the blood is usually mirrored in the milk — in cows as in humans — the milk of cows pregnant in the third trimester contains as much as twenty times as much estrogen found in milk from non-pregnant cows.

A new study in mice [16] tested whether the amount of estrogens found in regular dairy milk from pregnant cows had any effect on the circulating levels of estrogens and the genitals of the mice. After that, the mice were given times as much estrogen as they had found in the milk samples with the highest amount of estrogen. Only when the amount of estrogen reached times the amount found in milk, it became possible to detect effects on the blood and genitals. This observation is really no mystery: Everything that we absorb across the gastrointestinal membrane is transported directly to the liver through the portal vein system before it enters the general circulation.

That the liver is so effective at metabolizing steroid hormones is also the primary reason that bodybuilders usually have to inject steroids instead of ingesting them. If they do ingest them it is because the steroids have been chemically modified to be able to resist the passage through the intestines and liver, which is also the reason why ingestible steroids can have a toxic effect on the liver [18].

And that is really the real question we want answered — not whether certain hormones could theoretically raise our risk of cancer. If there was any strong evidence that milk raised the risk of cancer in general, it would be listed at the top of every article on the internet trying to persuade you or scare from drinking milk. You would see meta analyses of studies on milk that showed a clear connection between milk and cancer. Circumstantial evidence is ok to base our beliefs in when we have no other alternative.

But we do have alternatives. Figuring out of there is a connection between a specific food and cancer is much harder than many people assume. Even if we observe an association, it is not safe to assume that the one thing causes the other — it might as well be the other way around this is called reverse causality — which probably explains why artificially sweetened beverages and obesity are correlated [19] or it could be something else entirely that causes both the exposure and the outcome this is called a confounder.

Observe that an exposure and an outcome that seems connected, does not mean that one thing caused the other. When it comes to research into what raises the risk of cancer, we usually have nothing else than observations like these to go on.

We cannot make longitudinal controlled studies because it would be utterly unethical to try to actively provoke cancer in a group of people and if we did and saw even a small rise in cancer incidence, we would have to end the study immediately.

So how can we know whether something causes cancer or not? In Sir Austin Bradford Hill developed a set of criteria [20] that needs to be fulfilled for a causality between an assumed cause and effect to be established.

The Bradford Hill-criteria in summary looks like this:. A good example of an association that fulfills the Bradford Hill-criteria is smoking and lung cancer. The observed period of time between first exposure and the appearance of diagnosable cancer is congruent with what we would expect. There is a clear dose-response relationship more cigarettes lead to higher risk and there is a good explanation to what we observe, since cigarette smoke contains a long range of strong mutagens that is carcinogenic in both animal and cell studies.

To the best of my knowledge there is not a single food that fulfills the Bradford Hill-criteria for causality. To be able to claim that milk increases the risk of cancer, it would take among other things that milk consumption was consistently correlated with a marked increased risk of cancer and that this effect was dose dependent. Different studies point in different directions and with some types of cancers it seems like it is protecting against that specific type of cancer but seems to promote other types of cancer.

At least that is the focal point of the articles that through blatantly selective presentation of the literature reveals themselves as anti-milk ideologues. Maybe the observed correlations are causal. Maybe milk plays a small part in both protecting against some cancers, and promoting others. Why this relatively sudden growth? Are we evolving to greater heights, vertically speaking?

Before answering these questions, we need to remember that evolution requires two things: For example, finches that have large, powerful beaks also have an advantage cracking large, tough seeds during periods when small, soft seeds are scarce. As a consequence, large-beaked birds are more likely to eat better, survive longer and reproduce than small-beaked birds.

Because beak shape is an inherited trait one that is substantially influenced by genes , more successful reproduction by large beaked birds means that the genes predisposing finches to large beaks are transmitted to the next generation in relatively larger numbers than those genes encoding small beaks. Thus, the population of finches in the next generation will tend to have larger beaks than finches in their parent's generation. Let's use this basic operating principle of evolution to predict, retrospectively, the direction of change in human height if evolution were the cause of the change.

We know from studies conducted in industrial England that children born into lower socioeconomic classes were shorter, on average, than children born into wealthy families. We also know that poorer families had larger numbers of children. Given those initial conditions, what would evolution predict? The average population should have become shorter because the shorter individuals in the population were, from an evolutionary fitness perspective, more successful in passing on their genes.

But this did not happen. Instead, all segments of the population--rich and poor, from small and large families--increased in height. Thus, natural selection, the process whereby differences in reproductive success account for changes in the traits of a population, does not explain why we are taller. If evolution doesn't explain height increases, what does? Most geneticists believe that the improvement in childhood nutrition has been the most important factor in allowing humans to increase so dramatically in stature.

The evidence for this argument is threefold: First, the observed increase in height has not been continuous since the dawn of man; it began sometime around the middle of the nineteenth century. In fact, examinations of skeletons show no significant differences in height from the stone age through the early s. Also, during World Wars I and II, when hunger was a frequent companion of the German civilian population, the heights of the children actually declined.

They only recovered during the post-war years. Such data are consistent with recent research indicating that slow growth induced by temporary malnourishment can usually be reversed.

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