scholarly journals Lactose intolerance: myths and facts. An update

2022 ◽  
Vol 120 (1) ◽  
2016 ◽  
Vol 79 (7) ◽  
pp. 98-101
Іu.V. Marushko ◽  
T.V. Iovitsa ◽  
Yu.I. Todyka ◽  

Gunjan Kumari Katoch ◽  
Neegam Nain ◽  
Sawinder Kaur ◽  
Prasad Rasane

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1503
Millie Porzi ◽  
Kathryn J. Burton-Pimentel ◽  
Barbara Walther ◽  
Guy Vergères

Recent discoveries in the “omics” field and the growing focus on preventive health have opened new avenues for personalized nutrition (PN), which is becoming an important theme in the strategic plans of organizations that are active in healthcare, food, and nutrition research. PN holds great potential for individual health optimization, disease management, public health interventions, and product innovation. However, there are still multiple challenges to overcome before PN can be truly embraced by the public and healthcare stakeholders. The diagnosis and management of lactose intolerance (LI), a common condition with a strong inter-individual component, is explored as an interesting example for the potential role of these technologies and the challenges of PN. From the development of genetic and metabolomic LI diagnostic tests that can be carried out in the home, to advances in the understanding of LI pathology and individualized treatment optimization, PN in LI care has shown substantial progress. However, there are still many research gaps to address, including the understanding of epigenetic regulation of lactase expression and how lactose is metabolized by the gut microbiota, in order to achieve better LI detection and effective therapeutic interventions to reverse the potential health consequences of LI.

Gut ◽  
2021 ◽  
pp. gutjnl-2020-323911
M F Brandao Gois ◽  
Trishla Sinha ◽  
Johanne E Spreckels ◽  
Arnau Vich Vila ◽  
Laura A Bolte ◽  

2005 ◽  
Vol 88 (3) ◽  
pp. 157-202 ◽  
Anthony K. Campbell ◽  
Jonathan P. Waud ◽  
Stephanie B. Matthews

A staggering 4000 million people cannot digest lactose, the sugar in milk, properly. All mammals, apart from white Northern Europeans and few tribes in Africa and Asia, lose most of their lactase, the enzyme that cleaves lactose into galactose and glucose, after weaning. Lactose intolerance causes gut and a range of systemic symptoms, though the threshold to lactose varies considerably between ethnic groups and individuals within a group. The molecular basis of inherited hypolactasia has yet to be identified, though two polymorphisms in the introns of a helicase upstream from the lactase gene correlate closely with hypolactasia, and thus lactose intolerance. The symptoms of lactose intolerance are caused by gases and toxins produced by anaerobic bacteria in the large intestine. Bacterial toxins may play a key role in several other diseases, such as diabetes, rheumatoid arthritis, multiple sclerosis and some cancers. The problem of lactose intolerance has been exacerbated because of the addition of products containing lactose to various foods and drinks without being on the label. Lactose intolerance fits exactly the illness that Charles Darwin suffered from for over 40 years, and yet was never diagnosed. Darwin missed something else – the key to our own evolution – the Rubicon some 300 million years ago that produced lactose and lactase in sufficient amounts to be susceptible to natural selection.

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Mingyue Cheng ◽  
Zhangyu Cheng ◽  
Yiyan Yu ◽  
Wangjie Liu ◽  
Ruihao Li ◽  

Abstract Background Lactose malabsorption occurs in around 68% of the world’s population, causing lactose intolerance (LI) symptoms, such as abdominal pain, bloating, and diarrhea. To alleviate LI, previous studies have mainly focused on strengthening intestinal β-galactosidase activity while neglecting the inconspicuous drop in the colon pH caused by the fermentation of non-hydrolyzed lactose by the gut microbes. A drop in colon pH will reduce the intestinal β-galactosidase activity and influence intestinal homeostasis. Results Here, we synthesized a tri-stable-switch circuit equipped with high β-galactosidase activity and pH rescue ability. This circuit can switch in functionality between the expression of β-galactosidase and expression of L-lactate dehydrogenase in response to an intestinal lactose signal and intestinal pH signal, respectively. We confirmed that the circuit functionality was efficient in bacterial cultures at a range of pH levels, and in preventing a drop in pH and β-galactosidase activity after lactose administration to mice. An impact of the circuit on gut microbiota composition was also indicated. Conclusions Due to its ability to flexibly adapt to environmental variation, in particular to stabilize colon pH and maintain β-galactosidase activity after lactose influx, the tri-stable-switch circuit can serve as a promising prototype for the relief of lactose intolerance.

Cancer ◽  
1994 ◽  
Vol 74 (5) ◽  
pp. 1629-1633 ◽  
Howard L. Parnes ◽  
Eva Fung ◽  
Charles A. Schiffer

1999 ◽  
Vol 24 (1) ◽  
pp. 32-38 ◽  
Lois D McBean

2021 ◽  
Vol 67 (1) ◽  
Roberto CATANZARO ◽  
Morena SCIUTO ◽  
Birbal SINGH ◽  
Surajit PATHAK ◽  
Francesco MAROTTA

2021 ◽  
Vol 53 ◽  
pp. S171
A. Corea ◽  
T. Larussa ◽  
A.C. Procopio ◽  
C. Iannelli ◽  
A. Basile ◽  

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