“Based on numerous findings, we’ve discovered that the advice to have small babies and raise them to be big and strong is wrong. That’s because we’ve learned that nutritional status in pregnancy affects the future of not only the mother’s unborn child, but also her grandchildren’s generation.”<\/p>\n

Pointing out this fact is Professor Hisanori Kato of Japan Nutrition University, who is an expert in nutrigenomics (the study of nutrition’s effect on the genome) and epigenetic analysis. Over the course of many years, he has been shedding light on the mechanisms of how nutritional status in the womb affects the risk of lifestyle diseases after birth from an epigenetic perspective (we will explain more about epigenetics below).<\/p>\n

In 2006, the Ministry of Health, Labour and Welfare (MHLW) formulated the Dietary Guidelines for Pregnant and Lactating Women, which advised that, as a rough guide, women’s weight gain during pregnancy should be 9–12 kg for those of underweight (BMI of less than 18.5), 7–12 kg for those of a normal weight (BMI of at least 18.5 but less than 25.0), and around 5 kg for those with obesity (BMI of 25.0 or above), with advice tailored to the individual for those significantly beyond that level.<\/p>\n

“However, these guidelines didn’t circulate widely and weren’t thoroughly adhered to,” Kato says.<\/p>\n

In March 2021, the Japan Society of Obstetrics and Gynecology published a new set of guidelines: the Gestational Weight Gain Guidelines. While the recommended weight gain differs according to pre-pregnancy BMI, the lower limit was raised by 3 kg compared with the existing guidelines. Following on from this, the MHLW also revised the Dietary Guidelines for Pregnant and Lactating Women, raising the guide for weight gain during pregnancy. Thus, the guidance has shifted more toward recommending appropriate weight gain to prevent excessive thinness than was previously the case (Table 1).<\/p>\n

Table 1. <\/span>Guidelines on recommended weight gain in pregnancy (A–C) and recent Japanese research findings (D)<\/span><\/strong><\/div>\n\n<\/p>\n\n\n\n\n\n\n
<\/td>\n Source (name of organization, etc.)<\/td>\n Recommended weight gain^{1<\/sup><\/td>\n} Objective<\/td>\n<\/tr>\n
<\/tead><\/p>\n
A<\/th>\n U.S. Institute of Medicine (IOM) (2009)<\/td>\n BMI <18.5 (underweight): 12.7–18.1 kg
BMI 18.5–25 (normal): 11.3–15.9 kg
BMI 25–30 (overweight)^{2<\/sup>: 6.8–11.3 kg
BMI \u226530 (obese): 5.0–9.1 kg<\/td>\n} Appropriate birth weight^{3<\/sup><\/td>\n<\/tr>\n}
B<\/th>\n The Committee on Perinatology, Japan Society of Obstetrics and Gynecology (FY2021)<\/td>\n BMI <18.5 (underweight): 12–15 kg
BMI 18.5–less than 25 (normal weight): 10–13 kg
BMI 25–less than 30 (class 1 obesity): 7–10 kg
BMI \u226530 (class 2 obesity): Tailored to the individual (generally up to a maximum of 5 kg)<\/td>\n Minimize the risk of pregnancy complications<\/td>\n<\/tr>\n
C<\/th>\n MHLW^{4<\/sup>
Dietary Guidelines for Pregnant and Lactating Women Starting Before Pregnancy<\/td>\n} BMI <18.5 (underweight): 12–15 kg
BMI 18.5–less than 25 (normal weight): 10–13 kg
BMI 25–less than 30 (class 1 obesity): 7–10 kg
BMI \u226530 (class 2 obesity and above): Tailored to the individual (generally up to a maximum of 5 kg)<\/td>\n Minimize the risk of pregnancy complications<\/td>\n<\/tr>\n
D<\/th>\n Retrospective cohort study of 419,000 pregnant women in Japan<\/td>\n BMI <18.5 (underweight): 13.0–13.9 kg
BMI 18.5–less than 25 (normal weight): 11.0–11.9 kg
BMI 25–less than 30 (class 1 obesity): 8.0–8.9 kg
BMI \u226530 (class 2 obesity): Risk reduction plateaus at 5 kg<\/td>\n Minimize the risk of pregnancy complications<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<\/div>\n
\n
1 <\/div>\n
Uses a BMI (kg\/m2) calculated based on self-reported pre-pregnancy weight.<\/div>\n<\/div>\n
\n
2 <\/div>\n
A BMI of 25–30 kg\/m2 is considered overweight in the U.S. (classed as preobese in WHO standards), while a BMI of 30 kg\/m2 or above is considered obese.<\/div>\n<\/div>\n
\n
3 <\/div>\n
Sets a target of a birth weight of 3,000–4,000 g in the 39th–40th week of pregnancy.<\/div>\n<\/div>\n
\n
4 <\/div>\n
Since FY2021, the Children and Families Agency has overseen public awareness and related initiatives.<\/div>\n<\/div>\n
Source: Dietary Reference Intakes for Japanese (2025 edition, MHLW)<\/small><\/p>\n
Many studies have reported associations of maternal pre-pregnancy BMI and gestational weight gain with pregnancy complications and infant birth weight. A number of guidelines have been formulated based on these findings.<\/p>\n<\/div>\n<\/div>\n
Professor Kato cites the Developmental Origins of Health and Disease (DOHaD) hypothesis as a key concept for understanding the importance of preventing underweight in pregnancy.<\/p>\n
“Emerging in the 1980s, the DOHaD hypothesis is based on the idea that the environment during the fetal stage and in infancy determines the subsequent risk of lifestyle diseases,” he explains.<\/p>\n
Scientists have conventionally regarded lifestyle diseases as being caused by diet and lifestyle in adulthood. However, in the 1980s, British epidemiologist Dr. David Barker discovered that people who weighed less at birth (low birth weight infants) had a higher risk of dying of coronary artery disease, high blood pressure, and diabetes as adults. He argued that birth weight, a reflection of the intrauterine environment, influences health throughout life.<\/p>\n
“The case study best known for providing compelling support for this hypothesis is that of the Dutch Hunger Winter, which occurred toward the end of World War II.”<\/p>\n
A dramatically increased risk of developing lifestyle diseases<\/h2>\n
From the winter of 1944 until the beginning of 1945, during the final phase of World War II, the German army imposed a harsh blockade on food and fuel shipments to Amsterdam and other Dutch cities. Residents of those areas suffered such severe food shortages that they sought to stave off hunger by eating tulip bulbs, and around 20,000 people are said to have died of starvation.<\/p>\n
“In the 2000s, the results of decades-long studies of children born to women who were pregnant at that time began to be published,” Kato continues. “From these, we discovered that children born to mothers who had been through pregnancy during this stringent blockade had a dramatically increased risk of developing diabetes, hypertension, and other lifestyle diseases as adults.”<\/p>\n
Why do children born under conditions of nutritional deprivation later develop disease? Professor Kato explains the mechanism using the term “thrifty programming” (Figure 1).<\/p>\n
$\"\"$ <\/small><\/p>\n
Figure 1. <\/span>Mechanism of thrifty programming<\/span><\/strong>The mother rat\u2019s low-protein diet causes fetal undernutrition, producing offspring with high salt sensitivity and increased susceptibility to hypertension and stroke.<\/p>\n<\/div>\n
“Organisms are equipped with survival strategies to enable them to withstand harsh environments. When the mother’s body lacks adequate nutrition, the fetus predicts that food will continue to be scarce once it is born, so the infant is born with thrifty programming that will enable it to live even on small amounts of energy.”<\/p>\n
The fetus creates its body from a fertilized egg in accordance with its genetic information. And that is not all. The fetus receives environmental information from the mother’s body and adjusts its development in response. This means that if the mother is starving, the fetus will develop a body that readily stores energy and has a thrifty metabolism, because it interprets its environment as one in which food is scarce.<\/p>\n
“When children with thrifty programming are raised on an unexpectedly abundant diet after their birth, a mismatch occurs between their thrifty programming and their actual environment,” Kato says. “More specifically, it gives rise to catch-up growth.” <\/p>\n
If babies that were undernourished in the womb are fed abundant nutrients after being born, their bodies increase in weight and height at a rapid pace, in an effort to make up for their delayed growth. In other words, catch-up growth is a phenomenon whereby individuals whose growth had been temporarily delayed by undernutrition or illness, for example, demonstrate faster-than-normal growth after their nutritional status improves, in an effort to catch up to their original growth curve.<\/p>\n
This is a natural reaction that makes up for growth delays, and such individuals appear at first glance to be growing normally. However, this rapid catch-up can adversely affect future health.<\/p>\n
“That’s because, when there’s a sudden, large influx of nutrients into a body in the energy-conservation mode established by thrifty programming, the internal organs and metabolic functions can’t keep up, making the body more prone to insulin resistance and related metabolic abnormalities.”<\/p>\n
Among the different kinds of nutrients, intake levels of protein—the source of nutrition for building organs and other parts of the body—in particular are known to have a powerful influence in relation to DOHaD. In experiments on rats, Professor Kato investigated the effects of restricting protein during pregnancy.<\/p>\n
“In experiments using stroke-prone spontaneously hypertensive rats (SHRSP), pregnant rats were given either feed whose protein content had been halved or normal feed, and their offspring were raised to adulthood. Once those offspring had reached adulthood, we administered saline solution to all of them and compared their blood pressure changes and survival rates.” (Figure 2)<\/p>\n
$\"\"$ Modified from Otani, L. et al. Biosci. Biotechnol. Biochem.<\/i> 68, 488–494 (2004).<\/small><\/p>\n
Figure 2. <\/span>Blood pressure and survival following salt loading<\/span><\/strong>In experiments using SHRSP, the offspring and grand-offspring of dams fed either a low-protein diet or a normal diet were given saline to drink from 10 weeks of age. Both the offspring and grand-offspring of dams that were undernourished during pregnancy showed greater susceptibility to hypertension and died earlier.<\/p>\n<\/div>\n
Even the grandchildren developed high blood pressure and died early<\/h2>\n
A very clear difference emerged in the results of the experiments.<\/p>\n
The offspring in the group whose mothers were undernourished during pregnancy developed a markedly greater increase in blood pressure in response to the saline solution compared with the rats in the group whose mothers had received normal feed.<\/p>\n
In addition, those in the undernourished group suffered strokes earlier than the young rats in the group whose mothers had been well nourished during pregnancy and died in rapid succession.<\/p>\n
Professor Kato and his team also discovered that even where the offspring ate normal feed during their own pregnancies, if the “grandmother” rats had been undernourished during pregnancy, the grandchildren also developed higher blood pressure and died earlier.<\/p>\n
“In other words,” he says, “where rats are undernourished in the womb, their vulnerability to salt (salt sensitivity) is passed on to their own grandchildren’s generation.”<\/p>\n
Why does this occur?<\/p>\n
“When we investigated, we found that the kidneys and adrenal glands of the offspring of SHRSP rats fed a low-protein diet during pregnancy showed reduced expression of angiotensin receptor type 2 (AT_{2<\/sub>R), whose role includes lowering blood pressure and protecting blood vessels.”<\/p>\n}
Protein deficiency during fetal development in the womb would appear to be one cause of the decreased ability to properly control blood pressure even after birth.<\/p>\n
This gives rise to the same question. Why does this occur?<\/p>\n
“It appears to be diet-induced epigenetic changes,” Kato says.<\/p>\n
This refers to the acquired mechanism whereby diet controls the switches for gene expression (function) without altering the DNA base sequence (genetic information) in our bodies.<\/p>\n
“Our genes themselves don’t change,” he explains. “However, the foods and nutrients we consume, and habits such as when we eat, can turn our gene expression switches on or off.”<\/p>\n
He says research has confirmed that exposure to a low-protein environment at the fetal stage causes chemical changes called DNA methylation (a switch that regulates gene function) in the At2r gene in the kidneys, resulting in altered gene function (changes in mRNA expression).<\/p>\n
Professor Kato also explained a different example.<\/p>\n
“Undernutrition in the womb alters the DNA methylation state of a gene called Ptger1<\/i> in the kidneys. This change in methylation causes Ptger1<\/i> to become overactive. When salt is consumed later in life, the effects of the overactive Ptger1<\/i> impair sodium regulation, making the rats more prone to hypertension as a result.”<\/p>\n
High blood pressure has long been attributed to lifestyle and genes, but the results of these studies present the new perspective that the fetal environment is a factor contributing to individual differences in hypertension.<\/p>\n
Warning against simplistic food faddism<\/h2>\n
Based on the discussion so far, Professor Kato points out that there are two issues in need of improvement when it comes to nutritional guidance for pregnant women.<\/p>\n
The first is the setting of more appropriate target values for nutritional intake during pregnancy. For example, protein consumption during pregnancy is essential for maternal blood production and for fetal cell division and development. Accordingly, the MHLW’s Dietary Reference Intakes for Japanese (2020) recommends that women in the second trimester of pregnancy add an extra 5 g to the recommended intake of 50 g\/day for women aged 18 and older, rising to an extra 25 g during the third trimester of pregnancy.<\/p>\n
“There are two ways to measure protein: the nitrogen balance method (based on the quantity of nitrogen ingested and excreted) and the indicator amino acid oxidation method (based on the amino acid metabolic rate),” he explains. “Some have pointed out that the former underestimates the protein requirement to a quite substantial degree. As the figures set out by the MHLW are based on the nitrogen balance method, this suggests that the conventional protein requirement may be considerably lower than it should be.”<\/p>\n
In addition, a great deal of attention is now focusing on folate—a vitamin that is particularly crucial to normal fetal development—from a DOHaD perspective. However, in Japan, the fact that both the reference value and the actual level of intake are low is a problem.<\/p>\n
“I believe we should take steps to remedy the situation by reflecting the outcomes of DOHaD research in setting appropriate intake levels.”<\/p>\n
The second issue is ensuring that uniform nutritional guidance evolves into something more individualized. That is to say, the vision for the nutritional science of the future depicted by Professor Kato is precision guidance based on each individual’s data.<\/p>\n
“For example,” he continues, “nutritional guidance today is uniform, with everything lumped together in the categories of the second trimester or third trimester of pregnancy. However, we’d ideally provide optimal nutrition tailored to the individual by taking into account both their genotype and their current physical condition. We call this precision nutrition.”<\/p>\n
In recent years, services that analyze people’s individual genetic information have become increasingly accessible. These provide an understanding of an individual’s genetic makeup, ranging from everyday things like whether one has a high or low tolerance to alcohol, for example, to a person’s blood iron levels or allergy risk.<\/p>\n
“While the information in our genome remains unchanged throughout our lives, our epigenetics, gut flora, and data on such parameters as sleep and exercise change constantly. It would be great if we could achieve widespread availability of nutritional guidance based on monitoring these indicators in real time, using AI and the like to analyze them, and identifying the optimum diet for each individual at that particular moment.”<\/p>\n
However, the major barrier confronting us in this regard is cost. This is because providing personalized dietary guidance and meals based on this in hospitals and other contexts requires considerable expenditure on personnel, as well as effort.<\/p>\n
“We might find that implementation begins with meals for patients, or for athletes and others in fields requiring high performance levels,” Kato suggests.<\/p>\n
Nevertheless, he is hopeful about the prospects for implementing and popularizing this next generation of nutritional guidance. At the same time, however, it is a fact that when information on television shows or the internet suggests a food is good for our health, that food disappears from stores the very next day. Professor Kato cautions against this kind of simplistic food faddism.<\/p>\n
“When people hear that something is good for them, they tend to consume it to excess. What’s important is to lay the foundations by eating a well-balanced diet, and then adding things that are good for us on top of that.”<\/p>\n
So, what can we do to achieve this?<\/p>\n
“It’s vital to inform people of the evidence through education,” Kato says. “What’s also important is to understand the nature of one’s own genes, and to learn about one’s current state. That’s because doing so can help prevent diseases and enable us to take steps to lead a healthy life. And that won’t only benefit ourselves; it’ll also benefit our children and grandchildren.”<\/p>\n
Such next-generation nutritional guidance, based on epigenetics and precision nutrition, would enable registered dietitians to provide personalized nutritional guidance tailored to each individual’s background and grounded in scientific evidence. While cost and technological challenges remain, this is a highly desirable direction for the future.<\/p>\n
(Figures courtesy of Hisanori Kato)<\/small><\/div>\n","protected":false},"excerpt":{"rendered":"
It has long been conventional wisdom that women must not put on too much weight in pregnancy. Today, however, undernutrition and underweight during pregnancy in particular are posing a problem, because nutritional status in the womb could potentially have a major impact on the child’s future risk of developing lifestyle diseases. There are even reports that lack of protein at the fetal stage could place the child at risk of impaired blood pressure regulation later in life. Scientists believe that this is because the mother’s diet during pregnancy affects epigenetics, which controls gene function. It has also become apparent that the mother’s nutritional status can even affect her grandchildren.<\/p>\n","protected":false},"author":2,"featured_media":2704,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"footnotes":""},"categories":[15],"tags":[],"class_list":["post-2694","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-nutrition"],"acf":{"author":"text by Toshiko Mogi","intro":"
It has long been conventional wisdom that women must not put on too much weight in pregnancy. Today, however, undernutrition and underweight during pregnancy in particular are posing a problem, because nutritional status in the womb could potentially have a major impact on the child’s future risk of developing lifestyle diseases. There are even reports that lack of protein at the fetal stage could place the child at risk of impaired blood pressure regulation later in life. Scientists believe that this is because the mother’s diet during pregnancy affects epigenetics, which controls gene function. It has also become apparent that the mother’s nutritional status can even affect her grandchildren.<\/p>","person":[{"acf_fc_layout":"personcontent","personimg":2690,"personsholder":"Professor, Japan Nutrition University","personname":"Hisanori Kato","persondetail":"Graduated from the Department of Agricultural Chemistry at the University of Tokyo’s Faculty of Agriculture. He went on to obtain a Ph.D. in agriculture from the same institution in 1990. From 1991, he was a guest researcher at the U.S. National Institutes of Health’s National Institute of Diabetes and Digestive and Kidney Diseases Diabetes Branch. In 1993, he became an assistant professor at Utsunomiya University’s School of Agriculture, and was subsequently appointed an assistant professor at the University of Tokyo’s Graduate School of Agricultural and Life Sciences in 1999. In 2009, he took up the post of project professor at the University of Tokyo’s Organization for Interdisciplinary Research Projects before becoming a project professor at the same university’s Graduate School of Agricultural and Life Sciences in 2017. He has held his current role since 2023. In 2024, he received the Japanese Society for Amino Acid Sciences Award for Distinguished Investigator. He has authored many books, for general and specialist readers alike."}],"issue":2673,"custom_css":".entry-content .v297_feature01_04_table01_wrapper{\r\noverflow-x:auto;\r\noverflow-y:hidden;\r\n}\r\n.entry-content .v297_feature01_04_table01{\r\nborder:#666 solid 1px;\r\nborder-collapse:collapse;\r\nwidth:100%;\r\n}\r\n.entry-content .v297_feature01_04_table01 thead tr td{\r\nbackground-color:#eeeeef;\r\nborder:#666 solid 1px;\r\nfont-size:13px;\r\nfont-weight:normal;\r\nline-height:1.2;\r\npadding:.2rem .1rem;\r\ntext-align:center;\r\nvertical-align:middle;\r\n}\r\n.entry-content .v297_feature01_04_table01 tbody tr th,\r\n.entry-content .v297_feature01_04_table01 tbody tr td{\r\nbackground-color:#fceef4;\r\nborder:#666 solid 1px;\r\nfont-size:14px;\r\nfont-weight:normal;\r\nline-height:1.2;\r\npadding:.2rem .1rem;\r\ntext-align:left;\r\nvertical-align:middle;\r\n}\r\n.entry-content .v297_feature01_04_table01 tbody tr th{\r\nfont-size:18px;\r\ntext-align:center;\r\n}\r\n.entry-content .v297_feature01_04_table01 tbody tr:nth-child(even) th,\r\n.entry-content .v297_feature01_04_table01 tbody tr:nth-child(even) td{\r\nbackground-color:#fffde4;\r\n}\r\n.entry-content .v297_feature01_04_table01 tbody tr td:nth-of-type(2){\r\nwidth:28%;\r\n}\r\n.entry-content .v297_feature01_04_table01 tbody tr td:nth-of-type(3){\r\nwidth:50%;\r\n}\r\n.entry-content .v297_feature01_04_table01 sup{\r\ncolor:#990000;\r\nfont-size:xx-small;\r\nfont-weight:500;\r\n}\r\n.entry-content .v297_feature01_04_caption_wrapper{\r\nalign-items:flex-start;\r\ndisplay:flex;\r\nfont-size:x-small;\r\nfont-weight:normal;\r\njustify-cotent:flex-start;\r\nline-height:1.3;\r\ntext-align:left;\r\n}\r\n.entry-content .v297_feature01_04_caption_wrapper>div:first-of-type{\r\ncolor:#990000;\r\n}\r\n.entry-content .caption_sup{\r\nfont-size:xx-small;\r\n}\r\n"},"_links":{"self":[{"href":"https:\/\/healthist.net\/en\/wp-json\/wp\/v2\/posts\/2694","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/healthist.net\/en\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/healthist.net\/en\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/healthist.net\/en\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/healthist.net\/en\/wp-json\/wp\/v2\/comments?post=2694"}],"version-history":[{"count":0,"href":"https:\/\/healthist.net\/en\/wp-json\/wp\/v2\/posts\/2694\/revisions"}],"acf:post":[{"embeddable":true,"href":"https:\/\/healthist.net\/en\/wp-json\/wp\/v2\/issue\/2673"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/healthist.net\/en\/wp-json\/wp\/v2\/media\/2704"}],"wp:attachment":[{"href":"https:\/\/healthist.net\/en\/wp-json\/wp\/v2\/media?parent=2694"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/healthist.net\/en\/wp-json\/wp\/v2\/categories?post=2694"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/healthist.net\/en\/wp-json\/wp\/v2\/tags?post=2694"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}