Sunday, December 9, 2018

Inuit and vitamin D

Inuit mothers (Wikicommons - Ansgar Walk) - Inuit have low levels of vitamin D. Does this mean they're not getting enough? Or have their bodies adapted to an environment where it cannot easily be made in the skin or obtained from the diet?

Inuit people have "insufficient" vitamin D, even among those who eat a traditional diet and live a traditional lifestyle. There are consequently moves afoot to remedy this insufficiency by providing vitamin D supplements. In my opinion, this is a response to a largely nonexistent problem and will probably have adverse consequences.

My arguments are explained in an article I have just published in Inuit Studies. Here is the abstract:

Inuit have vitamin D blood levels that generally fall within the range of insufficiency, even when they live on a traditional diet of fish and game meat. Without this vitamin, bones soften and become deformed, a condition called rickets in children and osteomalacia in adults. Until recent times, however, this condition was much rarer among Inuit than among non-Inuit, even when the latter included people living near Inuit communities under similar conditions of climate and housing. This rarity was attributed to extended breastfeeding and a high-meat/low-cereal diet. The situation subsequently reversed, with Inuit becoming more at risk of developing rickets, first in Labrador during the 1920s and later elsewhere. To reduce this excess risk, researchers have recommended vitamin D supplementation, arguing that breast milk has too little vitamin D and that even a traditional diet cannot provide the recommended daily intake. We should ask, however, whether the problem is definitional. Inuit may have lower levels of vitamin D because they need less, having adapted culturally and physiologically to an environment where this vitamin is less easily synthesized in the skin. These adaptations include a diet that enhances calcium bioavailability (by means of ß-casein in breast milk, certain unknown substances in meat, and absence of phytic acid), as well as genetic changes that enable vitamin D to be used more efficiently. Although Inuit are today more at risk of developing rickets than are non-Inuit, this excess risk is nonetheless small and seems to have a dietary cause-namely, early weaning and abandonment of a high-meat/low-cereal diet.

Please feel free to offer comments or criticisms.


Frost, P. (2018). To supplement or not to supplement: are Inuit getting enough vitamin D? Études Inuit Studies 40(2): 271-291.

Sunday, December 2, 2018

More unintended consequences

Fond memories, by Raimundo de Madrazo y Garreta (1841-1920). The hormonal state of pregnancy causes women to have a lower capacity for multitasking and remembering future activities. What happens when oral contraceptives maintain this hormonal state for years and years?

In my last post I reviewed the literature on oral contraceptives and behavior. Women invest more in sexual attractiveness near the time of ovulation, putting on more makeup and sending out other visual, behavioral, and olfactory cues. Oral contraceptives seem to suppress this desire to be attractive.

Parallel to these attitudinal and behavioral changes over the menstrual cycle, we also find cyclical changes to certain brain regions:

[...] a large sample of 55 women was scanned three times along their menstrual cycle in concisely defined time windows of hormonal changes. Accordingly this is the first study using a large enough sample size to assess menstrual cycle dependent changes in human brain structure with sufficient power. Results confirm a significant estradiol-dependent pre-ovulatory increase in gray matter volumes of the bilateral hippocampus, but also show a significant, progesterone-dependent increase in gray matter volumes of the right basal ganglia after ovulation. No other areas were affect by hormonal changes along the menstrual cycle. These hormone driven menstrual cycle changes in human brain structure are small, but may be the underlying cause of menstrual cycle dependent changes in cognition and emotion. (Pletzer et al. 2018).

The same research team earlier reported differences in brain structure between oral contraceptive (OC) users and non-users. OC users were closer to men in their brain structure:

Men had larger hippocampi, parahippocampal and fusiform gyri, amygdalae and basal ganglia than women. Women showed larger gray matter volumes in the prefrontal cortex, pre- and postcentral gyri. These sex-dependent effects were modulated by menstrual cycle phases and hormonal contraceptives. We found larger volumes in the right fusiform/parahippocampal gyrus during early follicular compared to mid-luteal cycle phase. Women using hormonal contraceptives showed significantly larger prefrontal cortices, pre- and postcentral gyri, parahippocampal and fusiform gyri and temporal regions, compared to women not using contraceptives. (Pletzer et al. 2010).

This study was criticized because it made no distinction between progestin-only OCs and combined progestin/estradiol OCs. The results were quite different when another research team repeated this study with participants who used only the second type of pill. OC users now had less, not more, brain volume, particularly in certain regions of the cerebral cortex: 

In 90 women, (44 OC users, 46 naturally-cycling women), we compared the cortical thickness of brain regions that participate in the salience network and the default mode network, as well as the volume of subcortical regions in these networks. We found that OC use was associated with significantly lower cortical thickness measurements in the lateral orbitofrontal cortex and the posterior cingulate cortex. These regions are believed to be important for responding to rewards and evaluating internal states/incoming stimuli, respectively. (Petersen et al. 2015 - h/t to Wanda!)

These differing results may reflect the different types of OCs in use. Because progestin, like progesterone, has anti-estrogenic effects, long-term use would tend to masculinize a woman's brain; there is consequently more gray matter in the parahippocampal and fusiform gyri, which are likewise bigger in men than in women. In contrast, when women prevent conception by taking a mix of progestin and estradiol, which more closely mimics the hormonal state of pregnancy, certain regions of their cerebral cortex will tend to atrophy.


This atrophy may have an evolutionary cause. Keep in mind that a pregnant woman has to cope with a different pattern of cognitive demands: 

Pregnant women often have difficulty with multi-tasking and remembering future activities; however, they show improvement in memory for faces and recognition of emotional changes, particularly in men. They tend to have an increased sensitivity to odors, many of which are perceived as unpleasant. Perceptions of taste alter throughout pregnancy, with cravings for sweet foods in the second trimester and for salt in the third; sour tends to be preferred throughout the pregnancy. (Stadtlander 2013)

In general, the overall cognitive load is lower during pregnancy, so it makes sense that a pregnant woman’s body would allocate more resources to her developing child and fewer to her brain. The brain is, after all, the costliest organ of the human body, and it can probably cope with being a lower priority over the short term. Problems develop only if the hormonal state of pregnancy is artificially maintained for years and years.


Petersen, N., A. Touroutoglou, J.M. Andreano, and L. Cahill. (2015).Oral contraceptive pill use is associated with localized decreases in cortical thickness. Human Brain Mapping 36(7): 2644-2654. 

Pletzer, B., T. Harris, and E. Hidalgo-Lopez. (2018). Subcortical structural changes along the menstrual cycle: beyond the hippocampus. Scientific Reports 8: 16042

Pletzer, B., M. Kronbichler, M. Aichhorn, J. Bergmann, G. Ladurner, and H.H. Kerschbaum. (2010). Menstrual cycle and hormonal contraceptive use modulate human brain structure. Brain Research 1348: 55-62.

Stadtlander, L. (2013).  Memory and perceptual changes during pregnancy. International Journal of Childbirth Education 28(2): 49-53.