-
By using this site you agree to the terms, rules, and privacy policy.
-
Charlie's Restoration Giveaway #2 (Entire Home EMF Mitigation & Protection Along With Personal Protection) - Click Here To Enter
-
Dear Carnivore Dieters, A Muscle Meat Only Diet is Extremely Healing Because it is a Low "vitamin A" Diet. This is Why it Works so Well...
Rest the rest of this post by clicking here
-
The Forum is transitioning to a subscription-based membership model - Click Here To Read
Click Here if you want to upgrade your account
If you were able to post but cannot do so now, send an email to admin at raypeatforum dot com and include your username and we will fix that right up for you.
Article: How Goat's Milk Is Healthier Than Cow's Milk
- Thread starter Logan-
- Start date
I am not sure how reliable the studies sponsored by "a2 Milk Company Ltd." are. Still, I'll post them:
Nutr J. 2016; 15: 35.
Published online 2016 Apr 2. doi: [10.1186/s12937-016-0147-z]
PMCID: PMC4818854
PMID: 27039383
Effects of milk containing only A2 beta casein versus milk containing both A1 and A2 beta casein proteins on gastrointestinal physiology, symptoms of discomfort, and cognitive behavior of people with self-reported intolerance to traditional cows’ milk
Sun Jianqin,1 Xu Leiming,2 Xia Lu,
3 Gregory W. Yelland,4,5 Jiayi Ni,6 and Andrew J. Clarke7
Background
Dairy products, especially those derived from cows’ milk, are a major nutritional component and their consumption continues to increase worldwide. However, the increasing consumption of dairy products is associated with an increase in the risk of or the aggravation of symptoms of some disorders, including gastrointestinal dysfunction [1–5] and immune-/inflammation-related disorders [6, 7]. Some of these effects of dairy products have been attributed to a group of peptides present in milk derived from the proteolysis of β-casein, particularly β-casomorphin-7 (BCM-7).
BCM-7 is uniquely derived from the digestion of the A1 β-casein type but not the A2 β-casein type; the two primary types of β-casein present in milk. Either or both of these types may be expressed in cows’ milk depending on the individual cows’ genetic makeup. Cows may be homozygous for one type, or heterozygous with allelic co-dominance resulting in both types being expressed in milk. The two types differ in their protein structure owing to a substitution of the amino acid at position 67. A2 β-casein and related sub-variants including A3 and D contain a proline residue at this site whereas A1 β-casein and related sub-variants including B and C contain a histidine residue at this position, which allows the preceding seven amino acid residues to be cleaved, yielding BCM-7 [8]. Based on the β-casein structure and potential to yield BCM-7 upon digestion in humans, the β-caseins expressed in human, goat, sheep, and buffalo though not of the A2 type are classed as “A2-like”. It has been reported that casein and its derivatives, particularly BCM-7, exert a variety of effects on gastrointestinal function in animal models, including reducing the frequency and amplitude of intestinal contractions [3, 9–12], increasing mucus secretion [13–15], and suppressing lymphocyte proliferation [16, 17].
Intolerance to dairy products is a commonly reported gastrointestinal disorder, and is usually attributed to lactose intolerance [18]. However, based on the gastrointestinal effects of BCM-7 (and hence milk containing A1 β-casein), it is possible that intolerance to dairy products in some cases is related to the consumption of A1 β-casein rather than lactose per se. Our hypothesis is that the consumption of A1 β-casein leads to the production and exposure of tissue to BCM-7, which exerts a range of pro-inflammatory effects including altered signaling activity, redox disorders, and altered epigenetic regulation of gene expression [19]. A consequence of these changes is the disruption of digestive process, which may manifest as symptoms of lactose intolerance in terms of its presentation. Accordingly, the consumption of milk containing A2 β-casein at the exclusion of A1 β-casein may alleviate or prevent the gastrointestinal disturbances associated with BCM-7.
To date, however, few studies have compared the gastrointestinal effects of milk containing only the A2 β-casein type with milk containing A1 β-casein in humans [20]. Therefore, we performed a randomized, controlled, double-blind crossover study to compare the effects of milk containing only the A2 β-casein type with milk containing the A1 β-casein type in terms of gastrointestinal function, including serum and fecal laboratory tests, gastrointestinal symptoms of post-dairy digestive discomfort, stool frequency, Bristol Stool Scale, gastrointestinal transit time, and gastrointestinal inflammation. We hypothesized that the consumption of milk containing A1 β-casein would lead to systemic inflammation and gastrointestinal disorders similar to those of lactose intolerance in a cohort of subjects with perceived or confirmed lactose intolerance. We also hypothesized that elimination of the A1 β-casein type by providing subjects with milk that only contained the A2 β-casein type would avoid or attenuate these effects of A1 β-casein.
Because milk containing only the A1 β-casein type is not commercially available for consumption and is not representative of consumer milk products, we used normal milk containing a mixture of both the A1 and A2 β-casein types. Milk containing only the A2 β-casein type was confirmed to be prepared from cows homozygous for the A2 genotype.
We focused on a Chinese Han population because of the very high rate of perceived lactose intolerance or reported lactose malabsorption of up to 90 % in this population noted in some studies [21–23]. In spite of this, milk consumption in China has continued to increase, with per capita dairy product consumption among urban residents tripling from nearly 6 kg in 1992 to 18 kg by 2006 [24].
Abstract
Background
Cows’ milk generally contains two types of β-casein, A1 and A2 types. Digestion of A1 type can yield the peptide β-casomorphin-7, which is implicated in adverse gastrointestinal effects of milk consumption, some of which resemble those in lactose intolerance. This study aimed to compare the effects of milk containing A1 β-casein with those of milk containing only A2 β-casein on inflammation, symptoms of post-dairy digestive discomfort (PD3), and cognitive processing in subjects with self-reported lactose intolerance.
Methods
Forty-five Han Chinese subjects participated in this double-blind, randomized, 2 × 2 crossover trial and consumed milk containing both β-casein types or milk containing only A2 β-casein. Each treatment period was 14 days with a 14-day washout period at baseline and between treatment periods. Outcomes included PD3, gastrointestinal function (measured by smart pill), Subtle Cognitive Impairment Test (SCIT), serum/fecal laboratory biomarkers, and adverse events.
Results
Compared with milk containing only A2 β-casein, the consumption of milk containing both β-casein types was associated with significantly greater PD3 symptoms; higher concentrations of inflammation-related biomarkers and β-casomorphin-7; longer gastrointestinal transit times and lower levels of short-chain fatty acids; and increased response time and error rate on the SCIT. Consumption of milk containing both β-casein types was associated with worsening of PD3 symptoms relative to baseline in lactose tolerant and lactose intolerant subjects. Consumption of milk containing only A2 β-casein did not aggravate PD3 symptoms relative to baseline (i.e., after washout of dairy products) in lactose tolerant and intolerant subjects.
Conclusions
Consumption of milk containing A1 β-casein was associated with increased gastrointestinal inflammation, worsening of PD3 symptoms, delayed transit, and decreased cognitive processing speed and accuracy. Because elimination of A1 β-casein attenuated these effects, some symptoms of lactose intolerance may stem from inflammation it triggers, and can be avoided by consuming milk containing only the A2 type of beta casein.
Acknowledgments
This study was funded by The a2 Milk Company Limited. The authors thank Malav Trivedi, PhD (Nova Southeastern University) for providing technical support around methodologies, and Nicholas D. Smith, PhD (Edanz Group Limited), for medical writing support, which was funded by The a2 Milk Company Limited. The authors would also like to acknowledge the assistance of the clinical research organization S.P.R.I.M. China (Shanghai) Consulting Co., Ltd. for conducting the clinical trial.
Effects of milk containing only A2 beta casein versus milk containing both A1 and A2 beta casein proteins on gastrointestinal physiology, symptoms of discomfort, and cognitive behavior of people with self-reported intolerance to traditional cows’ milk
Nutr J. 2016; 15: 35.
Published online 2016 Apr 2. doi: [10.1186/s12937-016-0147-z]
PMCID: PMC4818854
PMID: 27039383
Effects of milk containing only A2 beta casein versus milk containing both A1 and A2 beta casein proteins on gastrointestinal physiology, symptoms of discomfort, and cognitive behavior of people with self-reported intolerance to traditional cows’ milk
Sun Jianqin,1 Xu Leiming,2 Xia Lu,
Background
Dairy products, especially those derived from cows’ milk, are a major nutritional component and their consumption continues to increase worldwide. However, the increasing consumption of dairy products is associated with an increase in the risk of or the aggravation of symptoms of some disorders, including gastrointestinal dysfunction [1–5] and immune-/inflammation-related disorders [6, 7]. Some of these effects of dairy products have been attributed to a group of peptides present in milk derived from the proteolysis of β-casein, particularly β-casomorphin-7 (BCM-7).
BCM-7 is uniquely derived from the digestion of the A1 β-casein type but not the A2 β-casein type; the two primary types of β-casein present in milk. Either or both of these types may be expressed in cows’ milk depending on the individual cows’ genetic makeup. Cows may be homozygous for one type, or heterozygous with allelic co-dominance resulting in both types being expressed in milk. The two types differ in their protein structure owing to a substitution of the amino acid at position 67. A2 β-casein and related sub-variants including A3 and D contain a proline residue at this site whereas A1 β-casein and related sub-variants including B and C contain a histidine residue at this position, which allows the preceding seven amino acid residues to be cleaved, yielding BCM-7 [8]. Based on the β-casein structure and potential to yield BCM-7 upon digestion in humans, the β-caseins expressed in human, goat, sheep, and buffalo though not of the A2 type are classed as “A2-like”. It has been reported that casein and its derivatives, particularly BCM-7, exert a variety of effects on gastrointestinal function in animal models, including reducing the frequency and amplitude of intestinal contractions [3, 9–12], increasing mucus secretion [13–15], and suppressing lymphocyte proliferation [16, 17].
Intolerance to dairy products is a commonly reported gastrointestinal disorder, and is usually attributed to lactose intolerance [18]. However, based on the gastrointestinal effects of BCM-7 (and hence milk containing A1 β-casein), it is possible that intolerance to dairy products in some cases is related to the consumption of A1 β-casein rather than lactose per se. Our hypothesis is that the consumption of A1 β-casein leads to the production and exposure of tissue to BCM-7, which exerts a range of pro-inflammatory effects including altered signaling activity, redox disorders, and altered epigenetic regulation of gene expression [19]. A consequence of these changes is the disruption of digestive process, which may manifest as symptoms of lactose intolerance in terms of its presentation. Accordingly, the consumption of milk containing A2 β-casein at the exclusion of A1 β-casein may alleviate or prevent the gastrointestinal disturbances associated with BCM-7.
To date, however, few studies have compared the gastrointestinal effects of milk containing only the A2 β-casein type with milk containing A1 β-casein in humans [20]. Therefore, we performed a randomized, controlled, double-blind crossover study to compare the effects of milk containing only the A2 β-casein type with milk containing the A1 β-casein type in terms of gastrointestinal function, including serum and fecal laboratory tests, gastrointestinal symptoms of post-dairy digestive discomfort, stool frequency, Bristol Stool Scale, gastrointestinal transit time, and gastrointestinal inflammation. We hypothesized that the consumption of milk containing A1 β-casein would lead to systemic inflammation and gastrointestinal disorders similar to those of lactose intolerance in a cohort of subjects with perceived or confirmed lactose intolerance. We also hypothesized that elimination of the A1 β-casein type by providing subjects with milk that only contained the A2 β-casein type would avoid or attenuate these effects of A1 β-casein.
Because milk containing only the A1 β-casein type is not commercially available for consumption and is not representative of consumer milk products, we used normal milk containing a mixture of both the A1 and A2 β-casein types. Milk containing only the A2 β-casein type was confirmed to be prepared from cows homozygous for the A2 genotype.
We focused on a Chinese Han population because of the very high rate of perceived lactose intolerance or reported lactose malabsorption of up to 90 % in this population noted in some studies [21–23]. In spite of this, milk consumption in China has continued to increase, with per capita dairy product consumption among urban residents tripling from nearly 6 kg in 1992 to 18 kg by 2006 [24].
Abstract
Background
Cows’ milk generally contains two types of β-casein, A1 and A2 types. Digestion of A1 type can yield the peptide β-casomorphin-7, which is implicated in adverse gastrointestinal effects of milk consumption, some of which resemble those in lactose intolerance. This study aimed to compare the effects of milk containing A1 β-casein with those of milk containing only A2 β-casein on inflammation, symptoms of post-dairy digestive discomfort (PD3), and cognitive processing in subjects with self-reported lactose intolerance.
Methods
Forty-five Han Chinese subjects participated in this double-blind, randomized, 2 × 2 crossover trial and consumed milk containing both β-casein types or milk containing only A2 β-casein. Each treatment period was 14 days with a 14-day washout period at baseline and between treatment periods. Outcomes included PD3, gastrointestinal function (measured by smart pill), Subtle Cognitive Impairment Test (SCIT), serum/fecal laboratory biomarkers, and adverse events.
Results
Compared with milk containing only A2 β-casein, the consumption of milk containing both β-casein types was associated with significantly greater PD3 symptoms; higher concentrations of inflammation-related biomarkers and β-casomorphin-7; longer gastrointestinal transit times and lower levels of short-chain fatty acids; and increased response time and error rate on the SCIT. Consumption of milk containing both β-casein types was associated with worsening of PD3 symptoms relative to baseline in lactose tolerant and lactose intolerant subjects. Consumption of milk containing only A2 β-casein did not aggravate PD3 symptoms relative to baseline (i.e., after washout of dairy products) in lactose tolerant and intolerant subjects.
Conclusions
Consumption of milk containing A1 β-casein was associated with increased gastrointestinal inflammation, worsening of PD3 symptoms, delayed transit, and decreased cognitive processing speed and accuracy. Because elimination of A1 β-casein attenuated these effects, some symptoms of lactose intolerance may stem from inflammation it triggers, and can be avoided by consuming milk containing only the A2 type of beta casein.
Acknowledgments
This study was funded by The a2 Milk Company Limited. The authors thank Malav Trivedi, PhD (Nova Southeastern University) for providing technical support around methodologies, and Nicholas D. Smith, PhD (Edanz Group Limited), for medical writing support, which was funded by The a2 Milk Company Limited. The authors would also like to acknowledge the assistance of the clinical research organization S.P.R.I.M. China (Shanghai) Consulting Co., Ltd. for conducting the clinical trial.
Effects of milk containing only A2 beta casein versus milk containing both A1 and A2 beta casein proteins on gastrointestinal physiology, symptoms of discomfort, and cognitive behavior of people with self-reported intolerance to traditional cows’ milk
Last edited:
Sponsored by: a2 Milk Company Ltd.
Nutr J. 2017 Oct 25;16(1):72. doi: 10.1186/s12937-017-0275-0.
Effects of cow's milk beta-casein variants on symptoms of milk intolerance in Chinese adults: a multicentre, randomised controlled study.
He M1, Sun J2, Jiang ZQ3, Yang YX4,5.
Author information
Abstract
BACKGROUND:
A major protein component of cow's milk is β-casein. The most frequent variants in dairy herds are A1 and A2. Recent studies showed that milk containing A1 β-casein promoted intestinal inflammation and exacerbated gastrointestinal symptoms. However, the acute gastrointestinal effects of A1 β-casein have not been investigated. This study compared the gastrointestinal effects of milk containing A1 and A2 β-casein versus A2 β-casein alone in Chinese adults with self-reported lactose intolerance.
METHODS:
In this randomised, crossover, double-blind trial, with a 3-day dairy washout period at baseline, subjects were randomised to consume 300 mL of milk containing A1 and A2 β-casein (ratio 58:42; conventional milk) or A2 β-casein alone; subjects consumed the alternative product after a 7-day washout period. Urine galactose was measured at baseline after a 15 g lactose load. Subjects completed 9-point visual analogue scales for gastrointestinal symptoms (borborygmus, flatulence, bloating, abdominal pain, stool frequency, and stool consistency) at baseline and at 1, 3, and 12 h after milk consumption.
RESULTS:
A total of 600 subjects were included. All six symptom scores at 1 and 3 h were significantly lower after consuming A2 β-casein versus conventional milk (all P<0.0001). At 12 h, significant differences remained for bloating, abdominal pain, stool frequency, and stool consistency (all P<0.0001). Symptom scores were consistently lower with A2 β-casein in both lactose absorbers (urinary galactose ≥0.27 mmol/L) and lactose malabsorbers (urinary galactose <0.27 mmol/L).
CONCLUSION:
Milk containing A2 β-casein attenuated acute gastrointestinal symptoms of milk intolerance, while conventional milk containing A1 β-casein reduced lactase activity and increased gastrointestinal symptoms compared with milk containing A2 β-casein. Thus, milk-related gastrointestinal symptoms may result from the ingestion of A1 β-casein rather than lactose in some individuals.
Trial registration
NCT02878876, registered August 16, 2016. Retrospectively registered.
Effects of cow’s milk beta-casein variants on symptoms of milk intolerance in Chinese adults: a multicentre, randomised controlled study
Nutr J. 2017 Oct 25;16(1):72. doi: 10.1186/s12937-017-0275-0.
Effects of cow's milk beta-casein variants on symptoms of milk intolerance in Chinese adults: a multicentre, randomised controlled study.
He M1, Sun J2, Jiang ZQ3, Yang YX4,5.
Author information
Abstract
BACKGROUND:
A major protein component of cow's milk is β-casein. The most frequent variants in dairy herds are A1 and A2. Recent studies showed that milk containing A1 β-casein promoted intestinal inflammation and exacerbated gastrointestinal symptoms. However, the acute gastrointestinal effects of A1 β-casein have not been investigated. This study compared the gastrointestinal effects of milk containing A1 and A2 β-casein versus A2 β-casein alone in Chinese adults with self-reported lactose intolerance.
METHODS:
In this randomised, crossover, double-blind trial, with a 3-day dairy washout period at baseline, subjects were randomised to consume 300 mL of milk containing A1 and A2 β-casein (ratio 58:42; conventional milk) or A2 β-casein alone; subjects consumed the alternative product after a 7-day washout period. Urine galactose was measured at baseline after a 15 g lactose load. Subjects completed 9-point visual analogue scales for gastrointestinal symptoms (borborygmus, flatulence, bloating, abdominal pain, stool frequency, and stool consistency) at baseline and at 1, 3, and 12 h after milk consumption.
RESULTS:
A total of 600 subjects were included. All six symptom scores at 1 and 3 h were significantly lower after consuming A2 β-casein versus conventional milk (all P<0.0001). At 12 h, significant differences remained for bloating, abdominal pain, stool frequency, and stool consistency (all P<0.0001). Symptom scores were consistently lower with A2 β-casein in both lactose absorbers (urinary galactose ≥0.27 mmol/L) and lactose malabsorbers (urinary galactose <0.27 mmol/L).
CONCLUSION:
Milk containing A2 β-casein attenuated acute gastrointestinal symptoms of milk intolerance, while conventional milk containing A1 β-casein reduced lactase activity and increased gastrointestinal symptoms compared with milk containing A2 β-casein. Thus, milk-related gastrointestinal symptoms may result from the ingestion of A1 β-casein rather than lactose in some individuals.
Trial registration
NCT02878876, registered August 16, 2016. Retrospectively registered.
Effects of cow’s milk beta-casein variants on symptoms of milk intolerance in Chinese adults: a multicentre, randomised controlled study
Last edited:
Nutrients. 2015 Sep; 7(9): 7285–7297.
Published online 2015 Aug 31. doi: [10.3390/nu7095339]
PMCID: PMC4586534
PMID: 2640436
Milk Intolerance, Beta-Casein and Lactose
Sebely Pal,1,* Keith Woodford,2 Sonja Kukuljan,3 and Suleen Ho1
Abstract
True lactose intolerance (symptoms stemming from lactose malabsorption) is less common than is widely perceived, and should be viewed as just one potential cause of cows’ milk intolerance. There is increasing evidence that A1 beta-casein, a protein produced by a major proportion of European-origin cattle but not purebred Asian or African cattle, is also associated with cows’ milk intolerance. In humans, digestion of bovine A1 beta-casein, but not the alternative A2 beta-casein, releases beta-casomorphin-7, which activates μ-opioid receptors expressed throughout the gastrointestinal tract and body. Studies in rodents show that milk containing A1 beta-casein significantly increases gastrointestinal transit time, production of dipeptidyl peptidase-4 and the inflammatory marker myeloperoxidase compared with milk containing A2 beta-casein. Co-administration of the opioid receptor antagonist naloxone blocks the myeloperoxidase and gastrointestinal motility effects, indicating opioid signaling pathway involvement. In humans, a double-blind, randomized cross-over study showed that participants consuming A1 beta-casein type cows’ milk experienced statistically significantly higher Bristol stool values compared with those receiving A2 beta-casein milk. Additionally, a statistically significant positive association between abdominal pain and stool consistency was observed when participants consumed the A1 but not the A2 diet. Further studies of the role of A1 beta-casein in milk intolerance are needed.
...
Given the specificity of A1 beta-casein to cattle of European origin, and hence also the release of BCM-7, the current evidence also provides a contributory explanation as to why some people report anecdotally that they can tolerate milk from mammals such as sheep [60] and goats (GenBank Accession No. AJ011019.3) (which contain A2-like beta-casein and not A1, because they have a proline at the homologous position on their beta-casein chains), but not cows. It is also clear that it is feasible for dairy farmers to breed herds of bovine cows that are free of A1 beta-casein. Indeed such herds already exist and, where available, the dairy products are supported by consumers.
Acknowledgments
Editorial assistance was provided by Sarah Williams and Helen Roberton of Edanz Group Ltd., which was funded by The a2 Milk Company.
Milk Intolerance, Beta-Casein and Lactose
Last edited:
Adv Nutr. 2017 Sep; 8(5): 739–748.
Published online 2017 Sep 7. doi: [10.3945/an.116.013953]
PMCID: PMC5593102
PMID: 28916574
Systematic Review of the Gastrointestinal Effects of A1 Compared with A2 β-Casein
Simon Brooke-Taylor,
Author information Copyright and License information Disclaimer
This article has been cited by other articles in PMC.
Go to:
Abstract
This is the first systematic review, to our knowledge, of published studies investigating the gastrointestinal effects of A1-type bovine β-casein (A1) compared with A2-type bovine β-casein (A2). The review is relevant to nutrition practice given the increasing availability and promotion in a range of countries of dairy products free of A1 for both infant and adult nutrition. In vitro and in vivo studies (all species) were included. In vivo studies were limited to oral consumption. Inclusion criteria encompassed all English-language primary research studies, but not reviews, involving milk, fresh-milk products, β-casein, and β-casomorphins published through 12 April 2017. Studies involving cheese and fermented milk products were excluded. Only studies with a specific gastrointestinal focus were included. However, inclusion was not delimited by specific gastrointestinal outcome nor by a specific mechanism. Inclusion criteria were satisfied by 39 studies. In vivo consumption of A1 relative to A2 delays intestinal transit in rodents via an opioid-mediated mechanism. Rodent models also link consumption of A1 to the initiation of inflammatory response markers plus enhanced Toll-like receptor expression relative to both A2 and nonmilk controls. Although most rodent responses are confirmed as opioid-mediated, there is evidence that dipeptidyl peptidase 4 stimulation in the jejunum of rodents is via a nonopioid mechanism. In humans, there is evidence from a limited number of studies that A1 consumption is also associated with delayed intestinal transit (1 clinical study) and looser stool consistency (2 clinical studies). In addition, digestive discomfort is correlated with inflammatory markers in humans for A1 but not A2. Further research is required in humans to investigate the digestive function effects of A1 relative to A2 in different populations and dietary settings.
...
Although His67 within A1 is susceptible to proteolytic cleavage, Pro67 within A2 is not. Thus, A1s have the potential to release short β-casomorphin (BCM) opioid peptides, including BCM-7, during gastrointestinal digestion (Table 1). The avoidance of A1 is feasible within dairy-based diets through the consumption of goat, sheep, and buffalo milk or through the consumption of bovine milk from the native Asian and African bovine breeds, or through the consumption of milk from genetically selected herds of European-type cattle that are certified free of the His67 mutation. Such herds are being developed in many countries.
...
Discussion
The evidence identified in this systematic review can be classified as a combination of conclusive (in which findings have been documented and found to be repeatable in different investigatory settings) and emerging (in which significant findings have been obtained, but where repeatability of findings in diverse research settings is required before the science can be regarded as settled). It is established that BCM-7 and related short BCMs (BCM-5, BCM-4, and BCM-3) are released by gastrointestinal digestion from the A1-type (but not the A2-type) β-caseins under in vitro conditions and in animals. Furthermore, these short BCMs exhibit direct μ-opioid receptor agonist activity both in vitro and in animal studies. In animals, there is consistent evidence that A1 slows gastrointestinal transit, and it is conclusive that this is opioid-mediated. A current clinical study also reported the release of pharmacologic quantities of BCM-7 in humans after the consumption of a quantity of bovine casein equivalent to 1 L of milk (28).
There is also consistent evidence in rodents that A1 and BCM-7 are proinflammatory and induce T cell–mediated immune response and emerging evidence of similar proinflammatory markers in humans. There is well-established previous evidence that endogenous μ-opioid agonists, such as β-endorphin, are released in the gut in response to chronic pain or injury and have signaling roles both neurologically and peripherally (46, 47). It is also well established that localized responses to endogenous opioid peptides in the gastrointestinal tract include alterations to gut motility and transit time (46, 48) and T cell–mediated inflammatory responses (49–51). Accordingly, the above effects from A1 and BCM-7 are consistent with a priori hypotheses.
Although the overall evidence for gastrointestinal effects from A1 and BCM-7 in animal trials and in vitro studies can be considered conclusive, the evidence from human clinical studies can be classed as emerging. Although there are strong theoretical grounds arising from the universality of μ-opioid receptors within mammalian gastrointestinal systems and the consistent evidence of β-casein effects on gastrointestinal transit to postulate that the gastrointestinal transit results from this specific milk-intolerant Han Chinese population will be repeatable with other population groups, such generalizability cannot be concluded without specific investigations thereof. It is also reasonable to postulate that longer gastrointestinal transit times may lead to increased effects of lactose fermentation and other dietary components, such as FODMAPS, which, together with genetic predisposition, may also be relevant in relation to clinical and subclinical outcomes, including both digestive discomfort and proinflammatory effects (3).
The 2 clinical studies in adult humans that investigated Bristol Stool Scale measures of fecal consistency both reported softer stools with A1 relative to A2, with one of these studies also showing softer stools associated with the A1 diet relative to a nondairy baseline diet. Although these results could be considered counterintuitive, given the delayed gastrointestinal transit and hence a perceived potential for possible constipation, they are consistent with the proinflammatory markers evident in both human and animal studies. However, given that these findings are counter to a conventional perception that longer transit will lead to constipation, further replication of these results is appropriate.
The published evidence in relation to A1 and gastrointestinal effects relates primarily to μ-opioid pathways. However, it is evident that A1 stimulates production of the enzyme DPP-4 in the rat jejunum through a nonopioid mechanism (39). It is also known that BCMs are 5-hydroxytryptamine2 (5HT2)-serotonin receptor antagonists through an unrelated mechanism (52–54). Furthermore, recent research has shown that A1 compared with A2 has implications for casein micelle structure and associated chaperone activity within the gastrointestinal system that is unrelated to opioid mechanisms (55). Accordingly, further research into these mechanisms within the human gastrointestinal system is warranted.
Within this study, we emphasize that our focus has been on a systematic analysis that draws on in vivo evidence—human and animal—supported by in vitro studies of underlying science. We wish to clearly distinguish between such a systematic study and a meta-analysis of human clinical studies, which would clearly be premature. We also acknowledge the likelihood that sensitivity to A1 may vary both across and within populations, with these issues yet to be elucidated.
In conclusion, it is evident that, under normal digestive conditions, the μ-opioid peptide BCM-7 is released from A1 but not from A2. There is extensive evidence from animal trials and emerging evidence in humans that this is associated with slower gastrointestinal transit and hence increased gastrointestinal transit times. It is also evident in animals and at least in some human population groups that the A1–derivative peptide BCM-7 is proinflammatory. The balance between the extent to which these effects are direct inflammatory responses to BCM-7, or indirect consequences of delayed transit influencing other biological processes, is yet to be elucidated. Although the current gastrointestinal evidence is strongly linked to BCM-7 and μ-opioid pathways, the possibility that some gastrointestinal effects involve nonopioid pathways is relevant. There is now a need for further clinical studies of A1 effects in a broad range of population groups (ages, ethnicities, and different genetic haplotypes) and dietary conditions.
Acknowledgments
We thank Oleg Sokolov for his advice in relation to the interaction of BCM-7 with the 5HT2-serotonin system. The authors’ responsibilities were as follows—SB-T: analyzed the data and had primary responsibility for the final content; SB-T and KW: designed and conducted the research; SB-T, KW, and KD: contributed to the writing of the manuscript; NK: reviewed the manuscript and provided relevant content; and all authors: read and approved the final manuscript.
Systematic Review of the Gastrointestinal Effects of A1 Compared with A2 β-Casein
Last edited:
Eur J Clin Nutr. 2014 Sep;68(9):994-1000. doi: 10.1038/ejcn.2014.127. Epub 2014 Jul 2.
Comparative effects of A1 versus A2 beta-casein on gastrointestinal measures: a blinded randomised cross-over pilot study.
Ho S1, Woodford K2, Kukuljan S3, Pal S1.
Author information
Abstract
BACKGROUND/OBJECTIVES:
At present, there is debate about the gastrointestinal effects of A1-type beta-casein protein in cows' milk compared with the progenitor A2 type. In vitro and animal studies suggest that digestion of A1 but not A2 beta-casein affects gastrointestinal motility and inflammation through the release of beta-casomorphin-7. We aimed to evaluate differences in gastrointestinal effects in a human adult population between milk containing A1 versus A2 beta-casein.
SUBJECTS/METHODS:
Forty-one females and males were recruited into this double-blinded, randomised 8-week cross-over study. Participants underwent a 2-week dairy washout (rice milk replaced dairy), followed by 2 weeks of milk (750 ml/day) that contained beta-casein of either A1 or A2 type before undergoing a second washout followed by a final 2 weeks of the alternative A1 or A2 type milk.
RESULTS:
The A1 beta-casein milk led to significantly higher stool consistency values (Bristol Stool Scale) compared with the A2 beta-casein milk. There was also a significant positive association between abdominal pain and stool consistency on the A1 diet (r=0.520, P=0.001), but not the A2 diet (r=-0.13, P=0.43). The difference between these two correlations (0.52 versus -0.13) was highly significant (P<0.001). Furthermore, some individuals may be susceptible to A1 beta-casein, as evidenced by higher faecal calprotectin values and associated intolerance measures.
CONCLUSIONS:
These preliminary results suggest differences in gastrointestinal responses in some adult humans consuming milk containing beta-casein of either the A1 or the A2 beta-casein type, but require confirmation in a larger study of participants with perceived intolerance to ordinary A1 beta-casein-containing milk.
Comparative effects of A1 versus A2 beta-casein on gastrointestinal measures: a blinded randomised cross-over pilot study
Comparative effects of A1 versus A2 beta-casein on gastrointestinal measures: a blinded randomised cross-over pilot study.
Ho S1, Woodford K2, Kukuljan S3, Pal S1.
Author information
Abstract
BACKGROUND/OBJECTIVES:
At present, there is debate about the gastrointestinal effects of A1-type beta-casein protein in cows' milk compared with the progenitor A2 type. In vitro and animal studies suggest that digestion of A1 but not A2 beta-casein affects gastrointestinal motility and inflammation through the release of beta-casomorphin-7. We aimed to evaluate differences in gastrointestinal effects in a human adult population between milk containing A1 versus A2 beta-casein.
SUBJECTS/METHODS:
Forty-one females and males were recruited into this double-blinded, randomised 8-week cross-over study. Participants underwent a 2-week dairy washout (rice milk replaced dairy), followed by 2 weeks of milk (750 ml/day) that contained beta-casein of either A1 or A2 type before undergoing a second washout followed by a final 2 weeks of the alternative A1 or A2 type milk.
RESULTS:
The A1 beta-casein milk led to significantly higher stool consistency values (Bristol Stool Scale) compared with the A2 beta-casein milk. There was also a significant positive association between abdominal pain and stool consistency on the A1 diet (r=0.520, P=0.001), but not the A2 diet (r=-0.13, P=0.43). The difference between these two correlations (0.52 versus -0.13) was highly significant (P<0.001). Furthermore, some individuals may be susceptible to A1 beta-casein, as evidenced by higher faecal calprotectin values and associated intolerance measures.
CONCLUSIONS:
These preliminary results suggest differences in gastrointestinal responses in some adult humans consuming milk containing beta-casein of either the A1 or the A2 beta-casein type, but require confirmation in a larger study of participants with perceived intolerance to ordinary A1 beta-casein-containing milk.
Comparative effects of A1 versus A2 beta-casein on gastrointestinal measures: a blinded randomised cross-over pilot study
D
Deleted member 5487
Guest
Better protein only 11% A1
Negative Pral- Potential Renal Acid load. Might even be the only protein source with positive on alkalinity. This would mean lower sulfur contain amino.
Feels far less sertongenic, actually dopminageric
More Fat, Naturall homogonized
I can never go back.
Negative Pral- Potential Renal Acid load. Might even be the only protein source with positive on alkalinity. This would mean lower sulfur contain amino.
Feels far less sertongenic, actually dopminageric
More Fat, Naturall homogonized
I can never go back.
GelatinGoblin
Member
- Joined
- Apr 15, 2020
- Messages
- 798
Bump
Thanks for the quote, i have only been drinking unhomogenized milk for the past 5+ years because it just tastes so much better. Previously i drank semi-skimmed milk because the whole milk when homogenized tastes like ***t. When unhomogenized it is delicious. My only wish regards to milk would be to find a source that does not pasteurize it, preserving it as RAW milk. I have no experience, but from what i have read it would be one of the few true superfoods.
I’ve drank fresh raw grass fed goat milk, as well as gently pasteurised, fasting both times and the result was still bad. For every claim that raw milk is a miracle healer/superfood you’ll find a person that was harmed by dairy, but everyone chooses to listen to the former
fasting is probably not the initial situation you want to start with consuming something so nutritionally dense. At least you should have limited intake to no more than deciliter per hour, did you? Fasting is easy, breaking the fast correctly is where the rubber meets the road.
I’m talking about an overnight fast, and then after drinking it waited a while (I think it was over an hour) till I ate something else. I warmed it up, sat down and drank the tiniest sips while making sure it stayed in my mouth a sufficient amount of time. Giant painful cystic acne and very quickly too. It’s an allergy. I assume I did it wrong by not completely destroying my gut bacteria first
lol, just assume you have destroyed your gut bacteria with your previous food decisions, and then introducing real food is a slight shock. Or alternatively you sourced bad milk, raw milk is much more sensitive to the quality of the producer than pasteurized milk, which in itself is quite sensitive in regards to outcome. You cannot consume ***t and expect other than ***t outcomes.
It wasn’t a ***t source, that mans goats were grazing in front of my front yard all summer long. And before I drank it I was a on a diet of grass fed beef, coconut and olive oil, tallow, bone broth, eggs and ripe fruits, spending nearly all my time in the sun. My own grandmother raised her goats and all they ate in the summer was pristine grass from the mountain. I remember how I urticaria from it as a kid. Casein is not for everyone, but if you thrive on it good for you. Won’t derail the thread any longer
as i said, if you have driven your body into a state called "lactose intolerance" or whatever mainstream likes to call it, you can get problems from milk before regaining balance. Same is true with all drastic changes in nutrition. Give 100g of carbs to a keto person and you will likely see them vomit.
My point was that unhomogenized milk is much less likely to cause problems than homogenized milk (from experience) and raw milk should be superfood (from what i have read).
My point was that unhomogenized milk is much less likely to cause problems than homogenized milk (from experience) and raw milk should be superfood (from what i have read).
GelatinGoblin
Member
- Joined
- Apr 15, 2020
- Messages
- 798
It's a matter of trial and error and seeing what works... If you could make that food digest for you it'd be great in theory
EMF Mitigation - Flush Niacin - Big 5 Minerals
Similar threads
