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    Issue Date: March 2024

    Lipid Droplets in Infant Formula Improve Child Neurodevelopment

    • Breastfeeding is positively associated with infant and child neurocognitive development.
    • Human breast milk and infant formula differ in their composition of milk lipids and in the structure of milk lipid globules. 
    • An experimental infant formula containing large lipid droplets coated with milk phospholipids, similar to what is found in human milk, positively affects child neurocognitive development. 

    Human breast milk has been positively associated with improving the neurodevelopment and function of children [1]. Breastmilk is considered the gold standard for infant nutrition; however, some parents are unable to breastfeed and must rely on infant formula. 

    Although it is a nutritious and effective substitute, infant formula does not perfectly mimic human milk. Infant formula is missing key sugars, lipids, and immune cells [2]. Some startup companies have made first attempts to produce human milk in a laboratory setting

    In a new clinical trial, published in Frontiers in Nutrition, researchers developed an infant formula that more closely mimics human milk by changing the size and structure of the lipid droplets in the new formula. They show that doing so can improve child neurocognitive development [3]. 

    Lidewij Schipper, a lead researcher on the study and a Principal Scientist in Nutrition and Brain Development at Danone Nutricia Research, says the new infant formula is “the first of its kind.”

    Human milk is produced in the mammary glands and contains bioactive elements such as dietary lipids. These lipids are organized into large droplets and are surrounded by a three-layered membrane called the milk fat globule membrane (MFGM). In contrast, infant formula contains small lipid droplets and no membrane, due to disruptions to the lipids during manufacturing [4]. 

    “The size and the membrane surrounding the lipid droplets affect how lipids from milk are digested and absorbed in the gastrointestinal tract,” says Schipper. “This may contribute to the growth and development of babies.”

    The researchers tested the new infant formula containing large lipid droplets that were surrounded by a single layer of milk phospholipids, which mimicked the outside layer of human milk fat globule membranes. They gave infants either standard or the new infant formula until 17 weeks of age during a random, double-blind trial. Breastfed babies were used as a reference [3].

    After 4 months, the scientists measured the babies’ blood lipid levels, specifically omega-3 and omega-6 long chain polyunsaturated fatty acids (LCPUFAs) [3]. “LCPUFAs are critical for brain growth and development,” Schipper says. “They can be found as structural components in neuronal cell membranes, and they have essential functional roles, for instance, contributing to neurotransmission.” Omega-3 LCPUFAs are particularly critical for supporting healthy neurodevelopment [5].

    The researchers found that the ratio of omega-6 to omega-3 in the blood was significantly higher in the standard formula group compared to the new formula and breastfed groups [3]. In other words, omega-3 levels were relatively lower in the standard formula group and relatively higher in the new formula and breastfed groups. This suggests that the large lipid droplets with the milk phospholipid membrane in the new infant formula may have improved the bioavailability for omega-3 LCPUFAs uptake in the baby’s brain.  

    The researchers then tested neurocognitive development every year from 3–5 years of age. They found that at 5 years old, children who were given the new formula showed better cognitive performance than those given standard formula. In fact, their cognitive function was closer to the breastfed group. According to Schipper, these results were not surprising, considering that the new formula was more like human milk. The relatively higher omega-3 LCPUFA levels observed with the new infant formula may have contributed to the differences in cognitive function [3].

    “Now that we have discovered that the size of lipid droplets and the presence of a membrane surrounding the lipid droplets in infant formula are functionally relevant,” says Schipper, “we can use this knowledge to the benefit of infants who receive infant formula.”

    The research group has additional ongoing clinical trials to confirm the benefits of this new infant formula. They are interested in conducting more long-term studies and analyzing the effects of the new formula on at-risk populations. In the future, they also plan to study the mechanisms underlying how the lipids affect neurocognitive development. 

    “Our expertise lies in the field of human milk research, which we’ve been studying for the past 50 years,” Schipper says. “We will keep conducting research and innovating because we believe in the power of nutrition to support babies’ growth and development.” 

    References

    1. Belfort MB, Rifas-Shiman SL, Kleinman KP, Guthrie LB, Bellinger DC, Taveras EM, et al. Infant feeding and childhood cognition at ages 3 and 7 years: Effects of breastfeeding duration and exclusivity. JAMA Pediatr. 2013;167(9):836–44.
    2. Martin CR, Ling PR, Blackburn GL. Review of infant feeding: Key features of breast milk and infant formula. Nutrients. 2016;8(5):1–11.
    3. Schipper L, Bartke N, Marintcheva-Petrova M, Schoen S, Vandenplas Y, Hokken-Koelega ACS. Infant formula containing large, milk phospholipid-coated lipid droplets and dairy lipids affects cognitive performance at school age. Front Nutr. 2023;10:1–11.
    4. Gallier S, Acton D, Garg M, Singh H. Natural and processed milk and oil body emulsions: Bioavailability, bioaccessibility and functionality. Food Struct. 2017;13:13–23.
    5. Colombo J, Carlson SE, Cheatham CL, Shaddy DJ, Kerling EH, Thodosoff JM, et al. Long-term effects of lcpufa supplementation on childhood cognitive outcomes. Am J Clin Nutr. 2013;98(2):403–12.

    Mammary Gland Organoids Reveal Species-specific Traits

    • Stem cells from diverse mammals can be grown in labs to form branched mammary gland organoids with lobes and ducts.
    • Culture conditions differ and reveal key growth factors necessary for some species but not others. 
    • Mammary gland organoids could help understand cancer susceptibility and factors that influence milk composition. 

    Mammary glands have evolved to produce a vast array of milks to support offspring. In ancient mammals such as monotremes, mammary glands are simply hairy patches. Some species of wallabies and kangaroos can produce distinct kinds of milk from different teats to support offspring of different ages. In humans and mice, these same glands take on elaborate structures with several ducts. These diverse paths to milk production have been difficult to study in laboratories, in part because of a lack of model systems. 

    In a new study [1], Gat Rauner, a developmental biology researcher at Tufts University in Boston, and her colleagues successfully cultivated 3-D organoids from mammary cells of several different species: one kind of opossum, cows, goats, hamsters, rats, rabbits, cats, ferrets, and pigs. 

    Rauner had wanted to study the mammary glands of diverse species ever since she learned as a graduate student that cows and other species were curiously resistant to cancer. “The mechanisms are really unknown and under-studied,” she said.  

    Such research has been challenging because of a lack of feasible laboratory models. Many species with different susceptibility or resistance to cancer are either wild or large animals and thus difficult to maintain in laboratories for studies. Mammary glands pose an additional hurdle because they undergo dramatic, temporary changes during lactation, which can be difficult to study in a laboratory if animals only reproduce infrequently or don’t do so in captivity. 

    If they could be grown, organoids would help circumvent the problem of needing an entire animal in the lab. But earlier attempts at producing mammary gland organoids from species other than humans and mice resulted in blobs of cells that lacked the characteristic features and functions of mammary tissue. “A lot of organoid models didn’t really have the morphology that is so characteristic of the mammary gland,” Rauner said.

    During her postdoctoral research, Rauner began collecting stem cells from mammary glands of various species. Nudging these cells to form glands requires a precise combination of growth conditions. Organoids from other species didn’t grow under the same culture conditions that work for stem cells from humans and mice. After many failed attempts, Rauner and her team discovered that tweaking the cell culture medium and the rigidity of the extracellular matrix, a gel-like support structure necessary for cells growth, was the key to success. 

    Using Intesticult, a growth medium designed to culture intestinal epithelial cells, worked best for all the species tested in this study, resulting in organoids with the branched, lobular- ductal structures seen in mature animals. When Rauner and her colleagues examined the ingredients of Intesticult individually, they found that components that inhibited the ROCK protein were important for stem cells to form branched structures. When grown in minimal media, opossum cells required the presence of the ROCK inhibitor to form branched organoids. This same culture condition caused human and rat stem cells to produce abnormal, hyper-branched organoids. Cow, goat, and rabbit organoids, on the other hand, required ROCK inhibition for successful growth. “By parsing out the specific needs of each species to activate the proper developmental program, we can learn what signals are necessary for each and compare that between species,” Rauner said. “In this sense, it’s the experimental process that teaches us about the biology.” 

    In the future, such models could also help study components of milk produced by different species at various stages of lactation, Rauner said. “We don’t actually have a good grasp of how milk composition is regulated,” she explained. Small sugary molecules known as oligosaccharides in milk are crucial modulators of an infant’s development and immune health. In humans, these molecules, known as human milk oligosaccharides (HMOs), mediate gut and brain development, predict allergy risk, and confer protection against infections. However, oligosaccharides are formed by modifying carbohydrates and proteins after synthesis, so their characteristics can’t be deduced by studying genetic or protein sequences. “You have to be able to collect them from milk and then look at them,” Rauner said. 

    Being able to secrete milk from organoids, collect it, and examine how different growth conditions impact oligosaccharides and other components could help researchers learn how milk composition is regulated – even in the absence of a live, lactating animal. “Having these organoids really opens up the possibility to study these questions without actually having access to the animals themselves,” Rauner said.

    References

    Kim HY, Sinha I, Sears KE, Kuperwasser C, Rauner G. Expanding the evo-devo toolkit: generation of 3D mammary tissue from diverse mammals. Development. 2024 Jan 15;151(2).

    Dairy at Breakfast Provides a Cognitive Boost

    • One of the many proposed health benefits of eating breakfast is short-term improvement in cognitive performance.
    • Two experimental studies found improvements in blood glucose levels, amino acid availability, feelings of fullness, and concentration when subjects consumed a dairy protein-rich breakfast compared with a carbohydrate-rich breakfast or skipping breakfast.
    • Dairy foods, including milk, cheese, and yogurt, have a low glycemic index and high protein content, which may be beneficial to cognitive functioning. 

    For every faithful breakfast eater, there is an equally devoted breakfast skipper unwilling to concede that it is the most important meal of the day. The science on the benefits of breakfast-eating is just as divided as the general public’s opinion. Although some studies have found regular breakfast eaters have a higher IQ or improved cognitive performance compared with those who frequently skipped the meal [1-6], other studies [7-9] found no relationship between breakfast-eating and cognitive capabilities. 

    One potential reason for these conflicting results is that most studies have been observational and considered only whether study subjects ate breakfast rather than what they ate for breakfast. From toast with jam, to eggs and ham, breakfast foods vary widely in nutrients that influence satiety (i.e., feeling full) and blood glucose levels, factors that are associated with cognitive performance [10]. When it comes to boosting brain power, not all breakfast foods are created equal—but which are optimal? Two new experimental studies [11, 12] highlight the important role of dairy in increasing satiety, regulating blood glucose levels, and improving cognitive concentration. 

    Just like our muscles need fuel for a workout, the brain requires energy—specifically, glucose—for memory and concentration. After an overnight fast, the body’s glucose stores are depleted. Breakfast replenishes the body’s glucose stores. Previous research [reviewed in 13, 14] suggests foods that have a low glycemic index provide the greatest benefit to cognitive performance. These  foods result in a lower blood glucose peak and stable levels of blood glucose over a longer period. 

    Carbohydrate-laden foods, like muffins, bagels, and donuts, provide plenty of glucose but do so in a quick spike followed by a drop in blood sugar levels—thus, they have a high glycemic index. Dairy foods, such as milk and yogurt, do contain carbohydrates but they have a low glycemic index because their carbohydrates are digested alongside milk proteins. 

    Whey proteins contain amino acids that have an insulin-stimulating effect that keeps blood sugar levels stable after a meal. In fact, these insulin-stimulating effects might even help limit glucose spikes from other sugar-filled foods consumed along with dairy [15]. Milk’s other protein class, casein proteins, plays an important role in maintaining a steady level of blood glucose. Whereas whey proteins are quickly broken down by digestive enzymes, caseins form an insoluble curd in the digestive tract, which slows digestion. In addition to promoting satiety, which can also impact concentration [10, 11, 13], slow casein digestion stimulates the production of gastric hormones that also can slow down the digestion (and therefore the transfer into the blood stream) of milk sugars [16]. 

    Dairy’s slow-digesting and insulin-stimulating proteins were tested against a carbohydrate-rich breakfast or no breakfast at all in two experimental studies [11, 12]. Both studies used a clever experimental approach called a crossover design. Rather than give one group of study subjects test meal A, another test meal B, and then compare the effects of meals A and B between subjects, crossover studies give each study subject meal A and meal B (or no meal at all) in random order and compare the effects of these meals within subjects. In doing so, crossover studies eliminate variability between subjects, such as in level of education, body mass, age, or daily caloric intake that can potentially influence metrics of interest like blood glucose levels or performance on a cognitive test. However, these studies are usually done over a short period of time, as human subjects could potentially gain weight and change their diet and lifestyle over months or years, and most definitely age over time. 

    In the first study [12], 20 healthy Dutch men and women between 20 – 40 years of age consumed three different test meals in random order. Test meals were consumed on the same day of the week and separated by either seven or 14 days as a “washout” period. The night before the test breakfast, all study subjects consumed the same standardized meal at 7:00pm. 

    The researchers tried to select test breakfasts like what a typical Dutch person might consume for breakfast, making sure that each meal was identical in total calories and total fat. Meal one was three slices of white bread, with a set amount of margarine (to stay dairy-free) and strawberry jam, along with black tea with sugar; meal two was identical to meal one except 250 ml of semi-skimmed cow milk replaced the black tea; meal three was three slices of white bread, 250 ml semi-skimmed cow milk, and 35 grams of low-fat Gouda cheese (this is The Netherlands, after all). 

    Results from blood samples taken at several intervals in the five hours after the test meal suggested that replacing carbohydrates (meal one) with one serving of dairy protein (meal two) increased the availability of amino acids and reduced the blood glucose response. Results also suggested that replacing carbohydrates with two servings of dairy (meal three) had these same effects plus increased satiety and an increase in the plasma concentration of glucagon-like peptide 1 (GLP-1), a hormone that promotes insulin secretion [12]. The increase in GLP-1 was believed to result from  an increase in both dairy protein and in calcium, suggesting that replacement with other protein types may not have the same physiological response. Unfortunately, this study did not measure cognitive performance, which has previously been linked to sustained glucose levels and increased plasma concentrations of amino acids, especially branched-chain amino acids like leucine that are found in high levels in dairy products [11].

    The second study [11] was conducted on 30 Danish women between the ages of 18 and 30 years old with a BMI >25 kg/m2 (the current metric used to identify someone as overweight or obese). The three test breakfast meals (again, assigned in random order) were a high-protein, low-carbohydrate meal (300 grams of high protein yogurt and 30 grams of oats), a low-protein, high carbohydrate meal (60 grams of whole grain bread with 30 grams of raspberry jam and 250 grams of apple juice), or no meal (only water). The meals (except for water) were matched for calories, fat, dietary fiber, and weight. Like the Dutch study, meals were selected for their familiarity with subjects. All meals were consumed at the study center after a 12-hr fast and participants had at least one day off in between each test meal for washout. Blood samples were collected before consuming the test meal, and then at regular intervals until 170 min after meal completion. Concentration (as a measure of cognition) was determined 150 min after meal completion using the paced auditory serial addition task (PASAT), which was probably about as fun to take as it sounds; 61 single-digit numbers were announced from an audio file every three seconds and participants added  the number to the previous one, saying the ongoing sum out loud [11].

    Subjects reported feeling more satiated and less hungry after consuming the dairy-protein rich breakfast compared with the carbohydrate-rich breakfast and no breakfast at all, despite no significant differences within-subjects across the three test meals in plasma levels of appetite-regulating hormones such as ghrelin [11]. Compared to their scores from the day without breakfast, participant PASAT scores improved on the high-protein test meal day but not the high-carbohydrate day. Although these results were not statistically significant, a 3.5% difference in scores from the same test taken at most two weeks apart seems noteworthy (keeping in mind the order of meals was random, and some participants had their high-protein meal first whereas others had it last—so you can’t account for “learning”). It would be worthwhile to repeat this type of study in a more heterogenous study population (both men and women, various body weights, various ethnic backgrounds) so the results could be extrapolated more widely. 

    Regardless, it is remarkable that in both the Dutch and Danish studies the researchers found within subject differences despite the subjects only consuming each test meal on one occasion and completing the study within the span of days and weeks, rather than months or years. It is estimated that nearly 25% of Americans regularly skip breakfast [17]. Some may skip because of lack of time, others for lack of hunger—but the results of these studies suggest that even eating breakfast with dairy foods like milk, yogurt or cheese on occasion could influence their health and mental acuity. And that goes for the other 75% of us that regularly eat breakfast, too. 

    References

    1. Liu J, Hwang WT, Dickerman B, Compher C. Regular breakfast consumption is associated with increased IQ in kindergarten children. Early Human Development. 2013 Apr 1;89(4): 257-62.
    2. Liu J, Wu L, Um P, Wang J, Kral TV, Hanlon A, Shi Z. Breakfast consumption habits at age 6 and cognitive ability at age 12: a longitudinal cohort study. Nutrients. 2021 Jun 17;13(6): 2080.
    3. Pollitt E, Mathews R. Breakfast and cognition: an integrative summary. The American Journal of Clinical Nutrition. 1998 Apr 1;67(4): 804S-13S.
    4. Mahoney CR, Taylor HA, Kanarek RB, Samuel P. Effect of breakfast composition on cognitive processes in elementary school children. Physiology & Behavior. 2005 Aug 7;85(5): 635-45.
    5. Yao J, Liu Y, Zhou S. Effect of eating breakfast on cognitive development of elementary and middle school students: An empirical study using large-scale provincial survey data. Medical Science Monitor: International Medical Journal of Experimental and Clinical Research. 2019;25: 8843.
    6. Leos-Urbel J, Schwartz AE, Weinstein M, Corcoran S. Not just for poor kids: The impact of universal free school breakfast on meal participation and student outcomes. Economics of Education Review. 2013 Oct 1;36: 88-107.
    7. Powell CA, Walker SP, Chang SM, Grantham-McGregor SM. Nutrition and education: a randomized trial of the effects of breakfast in rural primary school children. The American Journal of Clinical Nutrition. 1998 Oct 1;68(4): 873-9.
    8. McEwan PJ. The impact of Chile’s school feeding program on education outcomes. Economics of Education Review. 2013 Feb 1;32: 122-39.
    9. Sámano R, Hernández-Chávez C, Chico-Barba G, Córdova-Barrios A, Morales-del-Olmo M, Sordo-Figuero H, Hernández M, Merino-Palacios C, Cervantes-Zamora L, Martínez-Rojano H. Breakfast nutritional quality and cognitive interference in university students from Mexico City. International Journal of Environmental Research and Public Health. 2019 Aug;16(15): 2671.
    10. Edefonti V, Bravi F, Ferraroni M. Breakfast and behavior in morning tasks: Facts or fads? Journal of Affective Disorders. 2017 Dec 15;224: 16-26.
    11. Dalgaard LB, Kruse DZ, Norup K, Andersen BV, Hansen M. A dairy-based protein-rich breakfast enhances satiety and cognitive concentration before lunch in young females with overweight to obesity: A randomized controlled cross-over study. Journal of Dairy Science. 2023 Dec 21.
    12. Hilkens L, Praster F, van Overdam J, Nyakayiru J, Singh-Povel CM, Bons J, van Loon LJ, van Dijk JW. Graded Replacement of Carbohydrate-Rich Breakfast Products with Dairy Products: Effects on Postprandial Aminoacidemia, Glycemic Control, Bone Metabolism, and Satiety. The Journal of Nutrition. 2023 Dec 12.
    13. Galioto R, Spitznagel MB. The effects of breakfast and breakfast composition on cognition in adults. Advances in Nutrition. 2016 May;7(3): 576S-89S.
    14. Philippou E, Constantinou M. The influence of glycemic index on cognitive functioning: a systematic review of the evidence. Advances in Nutrition. 2014 Mar;5(2): 119-30.
    15. Frid AH, Nilsson M, Holst JJ, Björck IM. Effect of whey on blood glucose and insulin responses to composite breakfast and lunch meals in type 2 diabetic subjects. The American Journal of Clinical Nutrition. 2005. Jul 1; 82(1): 69-75.
    16. Kung B, Anderson GH, Paré S, Tucker AJ, Vien S, Wright AJ, Goff HD. Effect of milk protein intake and casein-to-whey ratio in breakfast meals on postprandial glucose, satiety ratings, and subsequent meal intake. Journal of Dairy Science. 2018 Oct 1;101(10): 8688-701.
    17. Buckner SL, Loprinzi PD, Loenneke JP. Why don’t more people eat breakfast? A biological perspective. The American Journal of Clinical Nutrition. 2016 Jun 1;103(6): 1555-6.

    Gene Variant May Give Milk Drinkers Lower Diabetes Risk

    • Studies exploring the link between milk intake and type 2 diabetes risk have shown conflicting results, but they seem to be population dependent, with a favorable effect in groups that tend to be lactose intolerant.  
    • In Hispanic or Latino people, the gene variants that control whether a person’s production of lactase, the enzyme that digests the sugar in milk, persists into adulthood are fairly evenly distributed. On average, those who are lactase-non-persistent (but not those who are lactase-persistent) showed a decreased risk in Type 2 diabetes risk. 
    • Increased milk intake in lactase-non-persistent people may boost the numbers of probiotic Bifidobacteria, which in turn may produce metabolites that protect against type 2 diabetes.  

    Drinking more milk may decrease the risk of type 2 diabetes (T2D) in people who carry a gene variant that prevents the production of lactase, the enzyme that digests the sugar in milk, in adulthood, according to a new study in Nature Metabolism [1]. The benefit appears to stem from milk’s ability to boost helpful bacteria in the gut microbiome, which may in turn increase levels of metabolites associated with a lower T2D risk. 

    Several studies have explored the link between milk intake and T2D risk [2-3]. Some found a protective association, but others didn’t, says Qibin Qi, a molecular epidemiologist studying metabolic diseases at the Albert Einstein College of Medicine in New York. A few even showed the opposite, that drinking milk increases T2D risk. “The results were controversial,” says Qi. “We really didn’t know what was going on.” 

    But he and his colleagues saw a clue: Meta-analyses showed that the effect of milk intake on T2D risk was population-dependent. Studies of Asian people tended to find a protective effect, but those of European non-Hispanic white people did not. Qi wondered whether that might track with whether the enzyme lactase, which breaks down the sugar in milk, persists into adulthood. Most people who lack the enzyme as adults struggle to digest milk. This trait is governed by two variants of a gene called LCT. The LCT variant that people carry is also population-dependent. The vast majority of East Asian people carry the lactase-non-persistent variant, whereas most non-Hispanic white European people carry the lactase-persistent variant [4]. “That led to our hypothesis that maybe these differences in association between milk intake and diabetes risk might be due to differences in these genotypes across different populations,” Qi says. 

    To test this hypothesis, he and his colleagues turned to a third group: people who identify as Hispanic or Latino. “The unique thing about this population is that the LCT genotype is quite balanced,” says Qi, with about 60% of Hispanic and Latino people carrying the lactase-non-peristent variant and 40% carrying the lactase-persistent variant. 

    The researchers investigated the link between milk intake and T2D risk in a long-term US national study called the Hispanic Community Health Study/Study of Latinos (HCHS/SOL). They analyzed data from 12,652 participants who contributed blood DNA samples and diet information to the study. Some of those participants also contributed fecal samples. Diet was assessed with a questionnaire about overall food intake and two surveys that asked participants to recall everything they consumed over the past 24 hours. In the lactase-non-persistent group, an increase in milk intake by just one serving in the two questionnaires was associated with a 30% decrease in the risk of developing T2D. 

    The researchers validated their results by probing the diet, genotype, and microbiome of participants in another large cohort called the UK Biobank Study. In that group, the effect was smaller, with milk intake pairing with a 15% decrease in T2D risk.

    Recent studies [5] have found that high milk intake was associated with an abundance of Bifidobacteria species, which have a strong probiotic effect. Here, Qi and his colleagues found that in the lactase-non-persistent participants (but not lactase-persistent participants), increased milk intake was associated with an increased number of all seven species of Bifidobacteria. This increase was also associated with a generally strong metabolic profile, consisting of features such as a lower fasting glucose level and lower amounts of adipose tissue. The researchers then examined the link between milk intake and metabolites in participants’ blood samples. In lactase-non-persistent participants, metabolites linked to a lower risk of T2D were present in higher numbers. 

    “One potential mechanism is that milk influences gut microbiota, and the gut microbiota may influence these metabolites,” Qi says. Certain species of gut bacteria, such as Bifidobacteria, may produce metabolites that the body itself doesn’t produce. In people who don’t generally consume much dairy—for example, because they struggle to digest it—that positive effect on Bifidobacteria levels may be stronger, which could explain why the effect of increased milk intake is higher. 

    Other explanations—for example, socioeconomic differences between different populations and differences in milk consumption—could be at play too, he says. 

    But a conundrum is that people who are lactase nonpersistent often have difficulty drinking more milk. “That’s the next question we really want to address,” Qi says. Some studies hint that people who don’t produce lactase could still drink milk if they introduce it very gradually. Doing so, perhaps accompanied by a probiotic containing Bifidobacteria, could potentially increase the numbers of those bacteria in the gut and thus enable lactose digestion. 

    “I don’t yet know how we will do that study,” says Qi. “We still need some detailed study designs for how to really help people to become lactose tolerant.” 

    References

    1. Luo K, Chen GC, Zhang Y, Moon JY, Xing J, Peters BA, Usyk M, Wang Z, Hu G, Li J, Selvin E, Rebholz CM, Wang T, Isasi CR, Yu B, Knight R, Boerwinkle E, Burk RD, Kaplan RC, Qi Q. Variant of the lactase LCT gene explains association between milk intake and incident type 2 diabetes. Nat Metab. 2024 Jan;6(1):169-186.
    2. Gijsbers L, Ding EL, Malik VS, de Goede J, Geleijnse JM, Soedamah-Muthu SS. Consumption of dairy foods and diabetes incidence: a dose-response meta-analysis of observational studies. Am J Clin Nutr. 2016 April;103(4):1111-24. 
    3. Alvarez-Bueno C, Cavero-Redondo I, Martinez-Vizcaino V, Sotos-Prieto M, Ruiz JR, Gil A. Effects of milk and dairy product consumption on type 2 diabetes: Overview of systematic reviews and meta-analyses. Adv Nutr. 2019 May;10(suppl_2):S154-S163. 
    4. Storhaug CL, Fosse SK, Fadnes LT. Country, regional, and global estimates for lactose malabsorption in adults: a systematic review and meta-analysis. Lancet Gastroenterol Hepatol. 2017 Oct;2(10):738-746.
    5. Kitaoka M. Bifidobacterial enzymes involved in the metabolism of human milk oligosaccharides. Adv Nutr. 2012 May;3(3):422S-9S. 

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