How Women Survive Breastfeeding
Breastfeeding should break down
mothers’ bones but it doesn’t.
Why not?
by Jerry Bergman, PhD
— In human anatomy, little details matter —
Introduction
Mammalian milk is composed of water, fat, lactose, calcium, whey proteins, and minerals in amounts that depend on the animal species.[1] Milk is very high in calcium for several very good reasons. Calcium deficiency (hypocalcemia) in infants causes major serious health problems including heart, nerve, and muscle function damage plus poor bone formation which causes brittle bones prone to fractures. Babies with low blood-calcium levels may have jittery, tremors or uncontrollable twitching.[2] It is also very important for development of teeth.
To meet the calcium requirement in breast milk, calcium is removed from maternal bones for milk production.
During early life, infants usually consume a diet dominated by milk. Breast-fed infants normally absorb adequate quantities of calcium and other minerals.[3] Breast milk contains the required calcium amount because in a mechanism active during breastfeeding, bones are stripped of calcium. This is caused specifically by the parathyroid hormone-related protein (PTHrP) which is the main driver for stripping calcium from maternal bones for milk production. In addition, estrogen levels, which helps to keep the bones healthy by regulating calcium intake, drops off precipitously during this time. [4] This potentially puts bones under tremendous stress.
Normal bone compared with bone with osteoporosis. From Wikimedia Commons.
An article in Nature on July 10 lists complications of osteoporosis, a disorder in which the bones become increasingly porous, brittle, and subject to fracture, owing to loss of calcium and other mineral components. It is sometimes resulting in pain, decreased height, and skeletal deformities, and occurs most often in elderly and postmenopausal women. Maintaining bone into old age illustrates the complexity of the calcium bone and breast milk maintenance system.
Osteoporosis significantly affects healthy aging and is commonly experienced by more women than men. Females produce estradiol (E2) is an anabolic hormone that regulates bone remodeling by increasing the number of osteocytes, osteoblasts and osteochondral skeletal stem cells. For women, estrogen depletion following menopause or anti-hormone therapies degrades bone mass, an effect that underscores the anabolic features of estrogen on bone. However, the intimate association between estrogen and bone is uncoupled during lactation when the E2 surge in late-stage pregnancy drops precipitously. Moreover, bone remodeling increases sharply in primates to meet the high calcium demand by progeny.[5]
The Evolutionary Narrative
What happened before humans and other mammals had a system for maintaining bone health in lactating mothers? The evolutionary explanation for the mechanism that ensures the mother’s milk is calcium-rich is related to the problem of infant death. Severe problems due to hypocalcemia were common, evolution postulates, until the right set of hundreds of mutations fortuitously evolved a new type of parathyroid hormone-related protein. This newly evolved protein removed calcium from the mother’s bones which is then incorporated into the mammary gland for use during milk production. The result of this set of new mutations was a significant reduction of death and disease in the offspring. Natural selection then allegedly caused our very early mammal ancestors lacking the mutation set to slowly be reduced in number due to disease, the narrative goes. The result was those mothers with the set of beneficial mutations eventually dominated the gene pool. From this ancient ancestor, we inherited the calcium-stripping mechanism.
The problem is, no evidence exists for this set of events which must have occurred very early in evolution because, as far as is known, the mechanism used to remove calcium from the bones is used in all mammals. Nor does anyone have scientific knowledge of the specific mutation set that produced the new design, partly because no known mammal lacks the required set of new mutations. Thus a pattern of evolutionary progress cannot be inferred.
Why Bones are Not Compromised From Calcium Removal
The continuous demand for calcium by newborns logically would eventually cause significant bone loss in mothers, resulting in mothers having major health problems. The maternal skeleton would obviously be severely compromised. Consequently, mechanisms must exist to prevent significant damage to the mother’s bones.[6] The level of calcium in the bones could theoretically drop as much as 30 percent in rodents due to the normal large litter sizes they have, and up to ten percent in humans.
Why bone strength is not seriously compromised when infant feeding occurred was unknown until now. An international team of 18 scientists from universities including UC Davis have identified a hormone that is produced in lactating mammals. The hormone promotes calcium buildup of bones, which keeps them strong during milk production.[7]
Corel Pro Photos
The newly discovered brain-derived hormone called the CCN3 circulatory factor is produced by ARCKISS neurons. CCN3 is an osteoanabolic hormone that is produced in both sexes. The specific action of this hormone involves stimulating human skeletal stem-cell activity, which in turn causes an increase in the bone remodeling rate, accelerating fracture repair. This new maternal brain hormone helps to ensure the survival of mammals.
The CCN3 mechanism was confirmed by injecting CCN3 hormone into injured mice. The results showed that CCN3 helped their bones to heal much faster than mice without the CCN3 factor.
Hope for Lactating Mothers
This finding is important in ameliorating bone-weakening conditions, such as osteoporosis, in humans. The scientists then set out to replicate osteoanabolic hormone identification in mutant female mice after first documenting that CCN3 circulates in the blood. CCN3 emerged as the top candidate, meeting all of the predicted benchmarks. Its secretion enhances bone formation and fracture repair, and its appearance coincides with the onset and loss of major bone disease traits. The relevance of brain-derived CCN3 in female physiology was also supported by demonstrating its essential role in lactating mothers. The authors summarize their data analysis:
In lactating mothers, the high calcium (Ca2+) demand for milk production triggers significant bone loss. Although estrogen normally counteracts excessive bone resorption by promoting bone formation, this sex steroid drops precipitously during this postpartum period. Here we report that brain-derived cellular communication network factor 3 (CCN3) secreted from KISS1 neurons of the arcuate nucleus (ARCKISS1) fills this void and functions as a potent osteoanabolic factor to build bone in lactating females.[8]
The discovery of CCN3’s role in promoting bone growth adds a layer of complexity to the mechanisms required to supply the needed level of calcium in breast milk while simultaneously ensuring the mother’s bone health.
Summary
A new hormone system was documented to ameliorate the loss of calcium in the mother’s bones that results from nursing a child, preventing the major health consequences of hypocalcemia. This system produces significant new level of complexity in the female hormone system. The CCN3 protein ensures that the mother’s bones maintain their strength while supplying the required level of calcium to the breast milk. It is one more discovery that adds to the known complexity of the mammalian body. And the more the functional complexity involved, the less the possibility of its evolution.
Evolutionists explain the evolution of this new complex system by postulating that the hypocalcemia problem in nursing mothers was common until a set of the right hundreds of mutations produced a new CCN3 hormone-related protein system. The result of this set of mutations was a significant reduction of disease in mothers. Natural selection then supposedly caused our very earliest mammal ancestor’s mother to be much healthier, resulting in those females with the beneficial set of mutations dominating the gene pool. From this ancient ancestor we inherited the mechanism designed to compensate for calcium loss in nursing mothers. This scenario is not based on any evidence, but rather supposition based on the evolutionary belief structure.
For more on breast milk, see my 10 Aug 2023 article, “Human Breast Milk Is Designed for Both Mother and Baby.”
References
[1] Pietrzak-Fiećko1, R., and A.M. Kamelska-Sadowska, “The comparison of nutritional value of human milk with other mammals’ milk,” Nutrients, 12(5):1404, May 2020.
[2] Berchtold, M., et al., “Calcium ion in skeletal muscle: Its crucial role for muscle function, plasticity, and disease,” Physiological Reviews 80(3):1215-1265, 2000.
[3] Lonnerdal, B., “Effects of milk and milk components on calcium, magnesium, and trace element absorption during infancy,” Physiological Reviews 77(3):643-669, 1997.
[4] Lonnerdal, 1997.
[5] Babey, M.E., et al., “A maternal brain hormone that builds bone,” Nature, https://doi.org/10.1038/s41586-024-07634-3, 10 July 2024.
[6] Babey, et al., 2024.
[7] Babey, et al., 2024.
[8] Babey, et al., 2024.
Dr. Jerry Bergman has taught biology, genetics, chemistry, biochemistry, anthropology, geology, and microbiology for over 40 years at several colleges and universities including Bowling Green State University, Medical College of Ohio where he was a research associate in experimental pathology, and The University of Toledo. He is a graduate of the Medical College of Ohio, Wayne State University in Detroit, the University of Toledo, and Bowling Green State University. He has over 1,900 publications in 14 languages and 40 books and monographs. His books and textbooks that include chapters that he authored are in over 1,800 college libraries in 27 countries. So far over 80,000 copies of the 60 books and monographs that he has authored or co-authored are in print. For more articles by Dr Bergman, see his Author Profile.
Recommended Resources:
See Illustra Media’s short film on the human skeleton (4 min).
Book: Your Designed Body by Glicksman and Laufmann.