Dieting Lifestyle

Podcast from: https://bengreenfieldfitness.com/podcast/low-carb-ketogenic-diet-podcasts/cancer-keto/

[0:00:00] Introduction

[0:00:51] About the Podcast and Guest

[0:01:49] Podcast Sponsor

[0:04:40] Audio Issue and Shownotes

[0:05:34] Guest Introduction

[0:08:43] The Heartwarming Story Behind How Dr. Axe Got into Natural Healing

H&C Food Inc of Brooklyn, NY is recalling the Frozen Fuzhou Fish Balls and the Fish Balls, because they may contain undeclared wheat, pork, egg, and crustacean. People who have an allergy or severe sensitivity to wheat, pork, egg and crustacean run the risk of serious or life-threatening allergic reaction if they consume these products.

The Fuzhou Fish Balls and the Fish Balls was distributed to supermarkets in Queens, NY and reached consumers mainly through the retail stores.

The recalling Frozen Fish Balls came with two different packages. First, the frozen fish balls are in the red and white plastic bag with gold and black font that are written Fish Balls and the size for this is NET WT: 14OZ (400g), UPC: 6 953006 4 50093. The Fuzhou Fish Balls are in the blue and white plastic bag with gold and white font that are written Fuzhou Fish Balls and there are two sizes: Net WT: 14 OZ (400g), UPC: 6 953640 050017 and Net WT:4.5 lbs. (2043g), UPC: 6 953640 05000. These Frozen Fish Balls don’t have the expiration date or lot code on the package, however, they can last for 18 months.

There are no illnesses have been reported to date.

The recall was initiated after it was discovered that product containing wheat, pork, egg and crustacean were distributed in packaging that did not reveal the presence of egg and crustacean. Subsequent investigation indicates the problem was caused by a temporary breakdown in the company's production and packaging processes.

Consumers who have purchased frozen fish balls are urged to return it to the place of purchase for a full refund. Consumers with questions may contact the company at 1-718-821-5188, from Monday – Friday 9 a.m. to 5 p.m.

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Stracciatella Ice Cream Biscuit [Vegan]

Ingredients

Preparation

Q: I'm a powerlifter who wants to know if using leg drive will help me bench press more weight. Some powerlifters dismiss it; others think it's the Holy Grail. What gives?

If leg drive isn't the Holy Grail, it's sitting right next to it on the kitchen counter. Here are the three most important things to know about using leg drive to increase your bench press:

• Pay attention to your foot position
• Harness every ounce of leg power
• Follow the "J" curve

Leg drive is whispered about in strength circles like it's some secret cure-all potion only the elite should have access to. Heaven forbid word should leak out to average folks struggling away in the gym! Sometimes the fitness industry has no shame.

Not that the value of the leg drive to a solid bench press is settled. One camp claims leg drive will turn bench press poodles into pit bulls, while another claims it's as useless as a pot of decaf.

I tend to fall into the former camp. First of all, keep in mind that the bench press is a full-body exercise. To lift the most weight, you need to remember your body is one complete system, one that includes your legs (and your hands). That's not to say good leg drive is all you need to turn a bench-pressing Pee-wee Herman into Jeremy "King of the Bench" Hoornstra. Even if it doesn't help you add a ton more weight to your bench, leg drive still will help you lift more safely. And if you don't believe that, just try doing a bench press with your legs up.

Pay Attention to Your Foot Position

Great bench press technique starts with the setup: finding the proper rack height, maintaining a tight upper back, setting your feet, and correctly positioning your hands and wrists. (I highly recommend watching Layne Norton's bench press technique tutorial to see a detailed breakdown of a properly-executed bench press.)

When setting up for a bench press, many lifters often overlook their foot position. This nuance is critical for insuring stability and maximum leg drive. Stance width is a personal preference but, generally speaking, the closer together your feet are, the easier it is to make the mistake of lifting your butt off the bench. Once that happens, you can pretty much kiss your lift goodbye.

I recommend finding a foot position for benching that puts your shins near vertical. If you have an extreme arch, you may want to set your feet way back underneath you and go up on your toes. In this position, you're trading maximal leg drive for a big arch. If you're an advanced lifter and can move more weight this way—and do it safely—run with it.

If you're able to take this stance with your feet flat, you'll develop the highest amount of tension in your upper body. This allows you to assume a stable position so you can generate the greatest amount of leg drive. If you're a shorter lifter who cannot get in this position, you're still in luck: Powerlifting meets allow shorter lifters to put platforms or plates under their feet. (Don't even think about getting your feet too close together in a powerlifting meet, though. Doing so for a contest lift is a universal violation of the alphabet soup of rules governing the powerlifting federations.)

Harness Every Ounce of Leg Power

Once you've established your footing, you can't just press your feet straight into the ground and do a hip thrust. Try that, and your butt will come off the bench. Instead, cue yourself to spread outward (like many folks do in the squat) and drive your toes into the front of your shoes as you press the barbell. Imagine that you're doing a leg extension with your feet flat on the floor.

As you drive your toes into the floor, imagine you're also trying to spread the floor apart with your feet. This technique will extend your hips without further extending your lumbar spine.

Follow the "J" Curve

In the past, I've talked about the desired J-curve bar path. Your leg drive should match this. Remember, you are initiating force backward toward the bar, not straight up, to have it complement the ideal bar path. Don't worry about pushing yourself off the bench. Your upper back is tight and dug into the bench so firmly you won't go anywhere.

Strong leg drive catalyzes tightness in the bench press and helps you start driving the barbell up off your chest from the bottom position. This is a huge advantage because the bench press follows an ascending strength curve: The muscle tension needed to move the weight decreases throughout the range of motion such that the lift will typically feel easier as you near full extension. Engaging your legs helps move the barbell the first couple inches off your chest. Once the bar is past that point, it will travel over the strongest pressing muscles. Following the J-curve path allows your chest, shoulders, and triceps to work together synergistically so you can lift the most weight.

Stretching does a whole lot of good for your body. It helps you avoid injuries, minimizes post-workout soreness, and can even improve your athletic performance. In fact, it’s so important that there are now entire boutique classes dedicated to it. But its benefits don’t just stop at your fitness routine—it can also majorly improve your sex life.

When you’re having fun between the sheets, you want to feel your best—and that means not dealing with cramps from being too tight during new positions or, you know, pulling a muscle. Plus, aside from being able to make your way through your Kama Sutra book pain-free to figure out what works best for you and your partner, you’ll also be able to strengthen your bond since increased flexibility can bring you closer together literally and figuratively.

If anyone knows how to improve your sex life through stretches alone, it’s some of your favorite fitness pros. And these are the best ones to start with.

Try these 9 stretches for better sex from 3 buzzy boutique fitness instructors.

1. Heart opener

“This is great to prepare the spine for an increase in range of motion, and maybe a hair whip or two. While standing, arch your back as far as you can. Drop your head back; hold for 3 seconds. Then, contract your body forward to round the spine. While dropping your head forward, hold for 3 seconds. This is preferably done to your favorite tune from the 50 Shades of Grey soundtrack.”

2. Goddess status

“This stretch is perfect to warm up your body for flexibility in your hips and inner thighs—and get you ready to finally attempt those tricky Kama Sutra positions. Starting in a typical runner’s stretch, take it a step further and bring your forearms down all the way to rest on the floor. Hold it for 30 seconds, if you can handle it.”

3. Libido lasso

“Feel your Kundalini rising from that root chakra, and get ready to cast a spell your lover will not soon forget. Standing with your feet wider than your hips, bend your knees, put your hands on your hips, and begin to create figure 8 formations using your hips. Press the hip front, then round it out toward the back, alternating sides as fast—and as long—as you like it.”

4. On top warm-up

“Get ‘on top’ of your game by making sure your quads are ready for some serious reps, you overachiever, you. On the ground, stretch one leg out, and bend the opposite leg to the side of you. As you’re comfortable, start to lean back to the floor behind you to feel the stretch. Extra credit if you can get your back all the way down on the floor. Hold it for 30 seconds.”

5. Cat cow

“Cat cow stretches the muscles in the back and belly, allowing for more movement in the spine. The movement also does work at the pelvis by tilting it in both directions.”

6. Lizard pose

“Lizard pose targets your hip flexor and groin and allows for more movement in the hips, including the ability to get lower in positions, such as a squat or lunge.”

7. Glute bridge

“Yes, the glute bridge strengthens the glutes, protecting the lower back, but double-whammy: When the glutes are activated in a glute bridge, it allows for a pretty sweet opening in the hip flexors due to the hip extension happening.”

Beth Cooke, yoga teacher and instructor at Sky Ting Yoga

8. Happy baby and malasana squat

“Happy baby and malasana squat are great for opening up the hips, which can make for a closer, deeper connection. These stretches are also good for helping you prevent hip cramps. Because there’s nothing worse than a road to orgasm roadblocked with a hip cramp.”

9. Tadasana

“Lifting the pelvic floor in a pose as simple as tadasana gives you great alignment and a sense of grounded confidence and power, which is helpful for sex and connects you to your sex organs, practicing radical embodiment.”

Now that you have your stretches done, try these workout moves for better sex. Or, meet the self-lubricating condom that promotes sexual health and peak friskiness.

One of the best decisions I’ve made when it comes to setting yearly goals is to set goals for more than just the standard areas, like improving your health or saving X amount of money for Y account. In 2017 and 2018, I had goals like playing X number of video games or reading X number of books or seeing how many new recipes I could make. These goals were fun, and even if I didn’t always 100% reach them, I still stuck with them throughout the year instead of giving up in despair sometime in February.

As you think about the money goals you want to set for 2019, look beyond goals that are strictly about finances. There are a number of goals you can set for your own personal development and enrichment that, as an added bonus, can also give your financial life a boost. Here three such goals to consider for next year:

1. Find new ways to expand your social life.

Hanging out with friends and family can get expensive fast, especially if busy schedules mean you end up doing get-togethers on short notice or have to meet up at a halfway point instead of doing something cheaper at home.

One of my friends came up with the idea to do a cooking club. Every month, someone in the group volunteers to demonstrate how to make a favorite dish, whether that’s chicken pot pie or paprikash or black bean and spinach enchiladas. We’ve even had people demonstrate simple cake decorating techniques or walk us through the basics of creating your own home garden. We schedule the cooking club weeks ahead of time because of busy schedules and small children, and since there are enough of us, we only need to volunteer maybe once or twice every year. The rest of the time, you get to show up to socialize, learn how to make a new thing, and eat for free.

Brainstorm what would work for you and your social circle. Maybe it’s a rotating movie night or a craft/DIY learning experience. Whatever it is, scheduling regular time to be with your friends in a low-cost, low-stress environment will help you improve your social life — and cut down on your socializing budget.

2. Make it a priority to learn something new.

I’m of the opinion that learning something new is a great way to keep from feeling like your life is going nowhere. And learning doesn’t have to be as structured or demanding as a school environment. It also doesn’t have to be expensive.

During my annual review, I asked my manager if our department had a budget for training. As it turns out, there is one! I’m now looking for local conferences and seminars that could be relevant to my position, and if I find something that sounds worthwhile, I’ll pass on the information on to my manager. Some of the places I’ve worked for also had tuition reimbursement, so it’s worth asking if there are similar opportunities for you to become more valuable to your company on their dime (and use that to leverage better compensation for yourself).

Local colleges frequently have classes for continuing education, as do many libraries. (Not to mention all the books in the library you can learn from.) One of my local grocery chains hosts cooking classes, and YouTube is filled with all kinds of educational videos, from how to do basic home maintenance repairs to how to budget an unpredictable income. Acquiring knowledge and developing skills are always worthwhile endeavors, and many of them can directly, or indirectly, help you either save money or learn to use it wisely. And if you do have the time, money, and desire for it, going back to school can be immensely helpful for your financial life, whether you want to make a transition to a better-paying industry or get the degree or certification you need to qualify for a higher salary.

3. Reassess your entertainment options.

If you’re anything like me, you have acquired more books than you’ve actually been able to read. I get it! There are just so many good books coming out all the time! And yet one-sixth of my bookshelf space is dedicated to books I’ve acquired and not yet read (and this is after purging my shelves earlier this year!). I also happen to be the queen of buying video games, getting to the point where you can explore the map freely, getting side-tracked by side quests, and then never finishing because I buy another game and start the cycle over. And don’t get me started on the movies I fell in love with in the theater, bought on DVD, and then never watched again.

I’m not normally someone who advocates for any kind of spending ban, but if you happen to be like me and hoard entertainment faster than you can consume it, it might be a good goal for you to enjoy what you already have (and give your wallet a breather). This year one of my goals was to read two books per month and to complete four video games, and I’m happy to say that I’ve already hit my book goal and made significant headway on my unread books. I’m only halfway through my video game goal, but I’ve also decided I’m not allowed to buy a new one until I finish an old one. (Kingdom Hearts III is out at the end of January, so I’ve got to get moving!)

Making a commitment to enjoy the entertainment I already own (and rereading/rewatching/replaying my favorites) will significantly reduce my entertainment costs, and I hope it will also make me more thoughtful with my new entertainment purchases.

*****

Whatever goals you decide to make for 2019, keep in mind the kind of goals that will help you enjoy your life — especially if they will have the added bonus of improving the state of your wallet.

Audrey is an editor and writer who spends her free time on young adult books and video games. You can reach her on Twitter or through her website.

Image via Unsplash

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Trial Registration  anzctr.org.au Identifiers: ACTRN12613000532707 and ACTRN12615000403538 and ClinicalTrials.gov Identifier: NCT02176122

Gram-negative bacteria that produce extended-spectrum β-lactamase (ESBL) enzymes are a global public health concern.1 Based on national surveillance data from 2011, the US Centers for Disease Control and Prevention estimated that ESBL producers accounted for at least 26 000 infections and 1700 deaths annually.2 A key feature of ESBL-producing Enterobacteriaceae is phenotypic resistance to oxyiminocephalosporins, in addition to penicillins.3 ESBL producers are increasingly commonplace in both community and health care settings.4 Carbapenems have been regarded as the treatment of choice for serious infections caused by ESBL producers.3,5 However, increased use of carbapenems may select for carbapenem resistance in gram-negative bacilli,6,7 which currently represents the greatest threat in terms of antibiotic resistance.

One strategy to reduce the global use of carbapenems could be to reevaluate alternative agents (ie, carbapenem-sparing regimens). β-Lactam/β-lactamase inhibitor (BLBLI) combination antibiotics, such as piperacillin-tazobactam, have been considered a carbapenem-sparing option for treatment of ESBL producers.8,9 ESBL enzymes are inhibited by tazobactam, and ESBL producers are frequently susceptible to BLBLIs in vitro.

Some observational studies have suggested that BLBLIs may be clinically effective for treating infections caused by ESBL producers,10-13 but conflicting results have been reported.14 This study aimed to test the hypothesis that a carbapenem-sparing regimen (piperacillin-tazobactam) is noninferior to a carbapenem (meropenem) for the definitive treatment of bloodstream infection (BSI) caused by ceftriaxone-nonsusceptible Escherichia coli or Klebsiella spp that test susceptible to piperacillin-tazobactam.

The trial protocol was developed by the Australasian Society for Infectious Disease Clinical Research Network and has been previously published.15 The full protocol is provided in Supplement 1. The protocol was designed to be pragmatic and reflect usual clinical care (PRECIS-2 diagram16; eFigure 7 in Supplement 2). The institutional review board for each recruiting center approved the protocol. Written informed consent was obtained from all patients or their appropriate representative. The results are reported in accordance with the CONSORT statement extension for Non-inferiority and Equivalence Trials.17

Patients were screened for enrollment in 26 hospitals in 9 countries (Australia, New Zealand, Singapore, Italy, Turkey, Lebanon, South Africa, Saudi Arabia, and Canada) from February 2014 to July 2017 (eFigure 3 in Supplement 2). Patients were stratified according to infecting species (E coli or Klebsiella spp; groups E or K), presumed source of infection (urinary tract or elsewhere), and severity of disease (Pitt bacteremia score ≤4 or >4). A high-risk stratum (E2 or K2) was defined by nonurinary source for BSI and Pitt score greater than 4 (eFigure 1 in Supplement 2).

Patients were randomly assigned to either meropenem or piperacillin-tazobactam in a 1:1 ratio according to a randomization list prepared in advance for each recruiting site and stratification. The sequence was generated using random permuted blocks of 2 and 4 patients, with the allocated drug revealed using an online randomization module within the REDCap data management system.18 All records were verified using double-data entry, with reference to the paper clinical record form.

All patients had a blood culture collected at day 3 after randomization or on any other day if febrile (temperature >38°C) up to day 5. Patients were followed up for 30 days after randomization, by telephone call if the patient was discharged from hospital. All patients had baseline clinical and demographic data recorded, as well as any antibiotics given up to 48 hours prior to initial positive blood culture and for 30 days after randomization. Clinical data were recorded daily from day of initial positive blood culture until day 5 after randomization (with day 1 being the day of randomization, which had to occur within 72 hours of initial blood culture collection) (eTable 1 in Supplement 2). On day 5, the primary treating team had the option to cease all antibiotics, continue the allocated agent or change to step-down therapy (eFigure 2 in Supplement 2).

The primary efficacy outcome was all-cause mortality at 30 days after randomization. Secondary outcomes included (1) time to clinical and microbiologic resolution of infection, defined as the number of days from randomization to resolution of fever (temperature >38.0°C) and leukocytosis (white blood cell count >12 000/μL; to convert to ×109/L, multiply by 0.001) plus sterilization of blood cultures; (2) clinical and microbiologic success at day 4 after randomization, defined as survival plus resolution of fever and leukocytosis plus sterilization of blood cultures; (3) microbiologic resolution of infection, defined as sterility of blood cultures collected on or before day 4 after randomization; (4) relapsed bloodstream infection, defined as growth of the same organism as in the original blood culture after the end of the period of study drug administration but before day 30 after randomization; and (5) secondary infection with a meropenem- or piperacillin-tazobactam–resistant organism or Clostridium difficile infection, defined as growth of a meropenem- or piperacillin-tazobactam–resistant gram-negative organism from any clinical specimen collected from day 4 after randomization to day 30 or a positive C difficile stool test in the setting of diarrhea. Adverse events were documented for each study group. Other BSI events (caused by organisms other than E coli or Klebsiella spp) were also recorded up to 30 days. For any missing repeated variable used to define clinical resolution (eg, daily white blood cell count), the last observation was carried forward until a new observation was recorded.

Bacteria isolated from blood cultures in enrolled patients were available for further analysis at the coordinating laboratory. Minimum inhibitory concentrations (MICs) for piperacillin-tazobactam and meropenem were determined by MIC test strips (bioMérieux and Liofilchem) and interpreted according to standards defined by the European Committee on Antimicrobial Susceptibility Testing (EUCAST).19 ESBL production was confirmed by combination disc testing with clavulanate.20 Whole-genome sequencing was performed as previously described21 (eTables 8-10 and eFigure 6 in the “Whole-Genome Sequencing Methods” section of Supplement 2) to determine sequence types (STs) and characterize β-lactamase genes.

Because no randomized clinical trials have previously compared treatment options for ESBL producers causing BSI, the sample size estimation was derived from the largest retrospective study available at the time.10 The overall 30-day mortality in this observational study was 16.7% in those receiving a carbapenem. Based on a mortality rate of 14% in the control group (assuming mortality in observational cohorts may be greater than in trials with exclusion criteria) and a noninferiority margin of 5%, 454 patients were needed in total to achieve 80% power with a 1-sided α level of .025, allowing for 10% dropout.22 A 5% noninferiority margin was chosen as the maximal difference in mortality between treatments that would be clinically acceptable, by consultation with infectious disease, critical care, and clinical trial specialists of the Australasian Society for Infectious Disease Clinical Research Network involved in the protocol development.15

The primary analysis population was defined as any correctly randomized patient receiving at least 1 dose of allocated drug and was used to make inference on noninferiority of the treatment group (piperacillin-tazobactam), compared with control (meropenem), in terms of the primary outcome (30-day mortality). This was supported by an analysis of the per-protocol (PP) population. Protocol deviations defining exclusion from the primary analysis and inclusion in the PP sample were adjudicated by an assessor blinded to treatment allocation. The proportions of deaths in the study groups were calculated, with absolute risk differences determined with the meropenem group as the reference. The Miettinen-Nurminen method (MNM) was used to determine 1-sided 97.5% CIs for risk differences.23 As a multisite study, alternate methods were also examined including score-based methods, which extend MNM24 and logistic regression with sites as fixed and random effects. Because the risk differences and confidence intervals for the primary and secondary outcomes were similar when estimated by MNM or logistic regression, results for the MNM are presented. Noninferiority of all-cause mortality at 30 days would be established if the upper bound of the 1-sided 97.5% CI did not cross the margin of 5%.

For secondary outcomes, parametric and nonparametric tests were used as appropriate, depending on whether the data were normally distributed. Because the secondary outcomes were considered exploratory, adjustments for multiple comparisons were not made. For secondary outcomes, statistical tests were 2-sided, with a P < .05 considered significant. An analysis of the primary end point was undertaken in prespecified subgroups: (1) urinary vs nonurinary source, (2) Pitt bacteremia score of 4 or greater or less than 4, (3) E coli vs K pneumoniae, (4) appropriate vs inappropriate empirical therapy, and (5) health care–associated vs non-health care–associated BSI. In addition, a post hoc analysis was undertaken of high-income vs middle-income countries (using Organization for Economic Cooperation and Development Development Assistance Committee definitions, http://www.oecd.org/dac) and patients with the presence or absence of immune compromise.

The homogeneity of treatment effects on the primary outcome was explored across subgroups using a test for the intervention by subgroup interaction by adding this term and the subgroup as covariates in a logistic regression model, using a 2-sided significance level of P < .05. To quantify the effect of missing data on secondary outcomes, a post hoc sensitivity analysis using multiple imputation was performed using multivariate imputation by chained equations for both discrete and continuous data,25 with computation via the ‘mice’ package in R version 3.5.0.26

Baseline patient characteristics were tabulated, with proportions for categorical variables, mean and SDs for normally distributed continuous variables, or median and interquartile ranges for skewed data. The influence of clinical variables other than randomized antibiotic therapy on the primary outcome was also explored in a multivariable logistic regression model, including the treatment group as an independent variable. Any variables associated with the primary outcome on bivariable analysis (2-sided P < .20) were included in a multivariable logistic regression model (ie, urinary tract source, Pitt score, Charlson Comorbidity Index score, Organization for Economic Cooperation and Development region, immune compromise, and health care–associated infection). The model was optimized using a step-wise approach, beginning with the bivariable model most strongly associated with the primary outcome. The goodness-of-fit of the model after each step was assessed using Akaike’s information criteria. Variables that did not improve the model fit were excluded. Adjusted odds ratios for the effect of the intervention on the primary outcome with 1-sided 97.5% CIs were calculated. Analysis of raw data to determine primary and secondary outcomes, including missing value imputation via last value carried forward where appropriate, was performed in R version 4.3.1,27 with subsequent statistical testing undertaken using Stata version 15.1 (StataCorp). The full statistical analysis plan is provided in Supplement 1.

A total of 1646 patients were screened during the trial period. Of these, 391 (23.8%) were randomized, although 12 patients (8 in the piperacillin-tazobactam group and 4 in the meropenem group) were randomized in error or did not receive the allocated study drug and were therefore excluded from the primary analysis population, which included 379 patients at baseline (191 received meropenem and 188 received piperacillin-tazobactam) (Figure 1). One patient who received piperacillin-tazobactam self-discharged against medical advice and was lost to follow-up, so the total number of patients who were evaluated for the primary outcome was 378. Baseline demographic and clinical details are summarized in Table 1. Overall, treatment groups were balanced with respect to baseline characteristics, although more patients in the meropenem group had diabetes (41.4% vs 31.4%), a urinary tract source for BSI (67.0% vs 54.8%), and higher APACHE II scores (21.0 vs 17.9). More patients in the piperacillin-tazobactam group had immune compromise (27.1% vs 20.9%) but had a shorter time to receipt of microbiologically appropriate antibiotics from onset of infection (5.5 hours vs 9.6 hours). By the day of randomization, 40.7% patients had resolved objective markers of infection (as defined in the secondary outcome measure of clinical and microbiological resolution), although this was similar between groups (40.3% in the meropenem group and 41.2% in the piperacillin-tazobactam group).

A total of 23 of 187 patients (12.3%) within the primary analysis population randomized to receive piperacillin-tazobactam as definitive therapy met the primary outcome of all-cause mortality at 30 days compared with 7 of 191 (3.7%) in the meropenem group (risk difference, 8.6% [1-sided 97.5% CI, −∞ to 14.5%]; P = .90 for noninferiority) (eFigure 4 in Supplement 2). Results were consistent within the PP population, with 18 of 170 patients (10.6%) meeting the primary outcome in the piperacillin-tazobactam group compared with 7 of 186 (3.8%) in the meropenem group (risk difference, 6.8% [one-sided 97.5% CI, −∞ to 12.8%]; P = .76 for noninferiority) (Table 2). Adjustment for a urinary tract source of infection and the Charlson Comorbidity Index score resulted in little change in the findings (unadjusted odds ratio, 3.69 [1-sided 97.5% CI, 0 to 8.82]; adjusted odds ratio, 3.41 [1-sided 97.5% CI, 0 to 8.38) (eTable 5 in Supplement 2).

Clinical and microbiological resolution by day 4 occurred in 121 of 177 patients (68.4%) in the piperacillin-tazobactam group compared with 138 of 185 (74.6%), randomized to meropenem (risk difference, −6.2% [95% CI, −15.5 to 3.1%]; P = .19) (Figure 2). The median day of resolution of signs of infection after randomization was 3 (interquartile range [IQR], 1,5) in the piperacillin-tazobactam group, and 2 (IQR, 1,5) in the meropenem group, but this difference was not significant (P = .18) (eFigure 5 in Supplement 2). There were also no significant differences in microbiological resolution by day 4 or rates of microbiological relapse, secondary infection with another multiresistant organism, or C difficile (Figure 2). Patients receiving piperacillin-tazobactam did not have significantly lower rates of subsequent detection of carbapenem-resistant organisms, although this event was infrequent (3.2% vs 2.1%) (Figure 2). The secondary outcomes were also consistent within the PP population. In subgroup analyses of the primary outcome within the primary analysis population, none of the tests for interaction were significant and none of the subgroups met the noninferiority margin. In addition, the direction of risk associated with randomization to piperacillin-tazobactam remained in favor of meropenem across all subgroups (Table 2). Multiple imputation analysis for missing values showed no differences in results for the analysis of secondary outcomes when compared with the last observation carried forward method (Missing Value Method Comparisons section and eTable 11 in Supplement 2).

Nonfatal serious adverse events occurred in 5 of 188 patients (2.7%) in the piperacillin-tazobactam group compared with 3 of 191 (1.6%) in the meropenem group. Details of all deaths and serious adverse events can be found in eTables 6 and 7 in Supplement 2.

A total of 306 isolates cultured from the blood of patients in the primary analysis population (80.7%) were available for microbiological analysis (n = 266 E coli and n = 40 K pneumoniae). The median piperacillin-tazobactam MIC was 2 mg/L (IQR, 1.5 mg/L to 4 mg/L). Twelve isolates (3.9%) tested nonsusceptible to piperacillin-tazobactam according to the EUCAST breakpoint for susceptibility (≤8 mg/L), although only 4 (1.3%) were nonsusceptible if the Clinical and Laboratory Standards Institute breakpoint (≤16 mg/L) was applied32 (eFigure 6 in Supplement 2). There was no significant difference in the median MICs of piperacillin-tazobactam between the treatment groups (P = .64), although the median MIC was significantly greater in K pneumoniae than E coli (4 mg/L vs 2 mg/L; P < .001). Most isolates (99.7%) tested susceptible to meropenem (median MIC, 0.023 mg/L; IQR, 0.016 mg/L to 0.032 mg/L; EUCAST breakpoint for susceptibility ≤2 mg/L). There was no clear relationship between piperacillin-tazobactam MIC and mortality in patients randomized to receive this drug (eTable 9 in Supplement 2). One K pneumoniae strain from Singapore (in a surviving patient randomized to meropenem) demonstrated high-level resistance to piperacillin-tazobactam (MIC ≥256 mg/L) via the presence of blaDHA-1 (AmpC-type β-lactamase). A single E coli strain from Turkey (from a surviving patient randomized to meropenem) demonstrated nonsusceptibility to meropenem (MIC, 4 mg/L) via blaOXA-162 (a variant of OXA-48 carbapenemase).

Phenotypic ESBL production was confirmed in 86.0% of isolates (85.0% of E coli and 92.5% of K pneumoniae). Whole-genome sequencing data were available for 293 (77.3%) of the initial blood culture isolates from patients in the primary analysis population. The dominant E coli multilocus ST was ST131 (56.8%), with a small number of multiple other STs represented. For K pneumoniae, no ST predominated, although ST25 (16.7%) and ST15 (11.1%) were most common. The K2 capsular serotype, associated with hypervirulence,33 was the most common serotype detected in 6 of 36 K pneumoniae infections (16.7%); no strains with K1 serotype were identified. ESBL genes were confirmed in 85.3% of isolates, with 10.2% possessing acquired ampC genes (predominantly blaCMY-2); 2.0% carried both ESBL and ampC. As previously described,21 the predominant ESBL genes were blaCTX-M-type (83.5%), with the most common subtypes being blaCTX-M-15 (54.5%), blaCTX-M-27 (13.0%), and blaCTX-M-14 (11.0%). The presence of narrow-spectrum oxacillinases (such as blaOXA-1 and variants) was also common (seen in 67.6% of all strains), and may compromise β-lactamase inhibition by tazobactam.34,35

A recent trial of meropenem-vaborbactam vs piperacillin-tazobactam for complicated urinary tract source found superiority of meropenem-vaborbactam over piperacillin-tazobactam for a composite end point of clinical cure or improvement and microbial eradication, even when few carbapenemase-producing strains (the target of the vaborbactam inhibitor component) were present.36 Whether piperacillin-tazobactam remains effective for urinary infections caused by ESBL producers in patients without BSI or low mortality risk remains uncertain. Efforts to define alternatives to carbapenems remain a priority. Whether newer BLBLI agents (such as ceftolozane-tazobactam or ceftazidime-avibactam) are useful options in this clinical context remains unknown and conclusions on the efficacy of new BLBLIs for these infections should not be drawn from the results of this trial before evaluation within randomized studies.

This study has several limitations. First, the inherent delays in the processing of blood cultures and susceptibility testing means that empirical therapy was not under control of the study team. Many patients (50/191, 26.2%) who were randomized to meropenem received a BLBLI empirically and, conversely, 13.8% (26/188) of those randomized to piperacillin-tazobactam received a carbapenem empirically (eTable 3 in Supplement 2). As empirical therapy may have a major influence on outcome, the fact that some “contamination” of drug exposure between the 2 groups exists may complicate inferences. However, this would tend to bias toward noninferiority. This pragmatic study was purposefully designed not to mimic registration drug trials, but to reflect clinical practice where prescribers are faced with a decision point when ceftriaxone nonsusceptibility is known. Second, step-down therapy (which was allowed on day 5 after randomization) with a carbapenem (eg, once-daily ertapenem) occurred in 20.1% (76/379) of all patients, even if randomized to piperacillin-tazobactam (eTable 3 in Supplement 2).

Third, whether adequate source control was achieved in patients with a complex source of BSI is not known and could have influenced mortality if imbalances were present. Fourth, although patients were recruited from diverse geographical and economic regions, only 2 patients were enrolled from North America (Canada), so it is possible that these results are not generalizable to the United States. However, E coli strains causing BSI in this study are consistent with the STs and their associated ESBL genes previously described as prevalent in the United States.37 Piperacillin-tazobactam may be dosed differently in some US hospitals than in this trial (eg, 3.375 g every 6 hours vs 4.5 g of 6 hours),14 but the lower dosing regimen has been associated with a low probability of achieving optimal drug exposure in ESBL producers.38 Extended or continuous infusions of piperacillin-tazobactam may optimize drug exposure but the clinical efficacy of this approach remains uncertain.39

Among patients with E coli or K pneumoniae bloodstream infection and ceftriaxone resistance, definitive treatment with piperacillin-tazobactam compared with meropenem did not result in noninferior 30-day mortality. These findings do not support use of piperacillin-tazobactam in this setting.

Corresponding Author: David L. Paterson, MBBS, PhD, University of Queensland Centre for Clinical Research, Faculty of Medicine, Bldg 71/918 Royal Brisbane & Women's Hospital Campus, Herston, QLD 4029, Australia ([email protected]).

Accepted for Publication: July 27, 2018.

Author Contributions: Drs Harris and Paterson had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. All authors have approved the final version of the manuscript.

Concept and design: Harris, Rogers, Iredell, Miyakis, Ingram, Athan, Lorenc, Peleg, Paterson.

Acquisition, analysis, or interpretation of data: Harris, Tambyah, Lye, Mo, Lee, Yilmaz, Alenazi, Arabi, Falcone, Bassetti, Righi, Rogers, Kanj, Bhally, Iredell, Mendelson, Boyles, Looke, Miyakis, Walls, Al Khamis, Zikri, Crowe, Ingram, Daneman, Griffin, Athan, Lorenc, Baker, Roberts, Beatson, Peleg, Harris-Brown, Paterson.

Drafting of the manuscript: Harris, Lorenc, Roberts, Harris-Brown, Paterson.

Critical revision of the manuscript for important intellectual content: Harris, Tambyah, Lye, Mo, Lee, Yilmaz, Alenazi, Arabi, Falcone, Bassetti, Righi, Rogers, Kanj, Bhally, Iredell, Mendelson, Boyles, Looke, Miyakis, Walls, Al Khamis, Zikri, Crowe, Ingram, Daneman, Griffin, Athan, Baker, Beatson, Peleg, Harris-Brown, Paterson.

Statistical analysis: Harris, Baker.

Obtained funding: Harris, Mo, Ingram, Harris-Brown, Paterson.

Administrative, technical, or material support: Harris, Tambyah, Lye, Mo, Yilmaz, Arabi, Righi, Rogers, Iredell, Boyles, Walls, Crowe, Daneman, Lorenc, Harris-Brown, Paterson.

Supervision: Harris, Lye, Alenazi, Arabi, Kanj, Bhally, Miyakis, Walls, Al Khamis, Zikri, Athan, Beatson, Peleg, Harris-Brown, Paterson.

Conflict of Interest Disclosures: All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Harris reported receiving grants from the Australian Society for Antimicrobials; the International Society for Chemotherapy; the National University Hospital Singapore; the Study, Education, and Research Committee of Pathology; and the Royal College of Pathologists of Australasia Foundation. Dr Harris also reported receiving support to speak at an educational event sponsored by Pfizer. Dr Tambyah reported receiving grants from the National University Health System, GlaxoSmithKline, Janssen, Shionogi, Sanofi-Pasteur, Visterra, Baxter, ADAMAS, Merlion Pharmaceuticals, Fabentech, and Inviragen. He has also received honoraria from Novartis and AstraZeneca. Dr Falcone reported receiving personal fees from MSD, Angelini, and Astellas and grants from Gilead. Dr Bassetti reported receiving grants and/or personal fees from Pfizer, MSD, Astellas, Menarini, Roche, Tetraphase, Achaogen, Angelini, AstraZeneca, Bayer, Basilea, Cidara, Gilead, MSD, Paratek, Pfizer, The Medicines Company, and Vifor. Dr Rogers reported receiving grants and personal fees from MSD Australia for attending advisory boards and research and personal fees from Mayne Pharma for consulting. Dr Kanj reported receiving honoraria for speaking and serving on advisory boards for Pfizer, Merck, Bayer, Gilead, Hikma, and Aventis. Ms Lorenc reported receiving grants from the Australian Society for Antimicrobials, the International Society for Chemotherapy, and the National University Hospital Singapore. Dr Beatson reported receiving support for speaking at an educational event sponsored by Pfizer. Dr Peleg reported receiving grants from MSD. Dr Paterson reported receiving grants and/or personal fees from Merck, Pfizer, Shionogi, Achaogen, AstraZeneca, Leo Pharmaceuticals, Bayer, GlaxoSmithKline, and Cubist. No other disclosures were reported.

Funding/Support: The study was sponsored by the University of Queensland. This study was funded by grants from the Australian Society for Antimicrobials (ASA), International Society for Chemotherapy (ISC), National University Hospital Singapore Clinician Researcher Grant NUHSRO/2014/121/CRG/07. Whole-genome sequencing was funded by grants from the Australian Infectious Disease Centre and Australian Genome Research Facility; the Royal College of Pathologists of Australasia (RCPA) Foundation; and the Study, Education, and Research Committee (SERC) of Pathology Queensland. Dr Beatson was supported by a National Health and Medical Research Council (NHMRC) Career Development Fellowship during the course of the trial. Dr Harris was supported by an Australian Postgraduate Award from the University of Queensland. Dr Peleg was supported by a NHMRC Career Development and Practitioner Fellowship during the course of the trial. Dr Paterson was supported by a NHMRC Practitioner Fellowship during the course of the trial.

Role of the Funder/Sponsor: The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.

Group Information: The MERINO Trial Investigators and the Australasian Society for Infectious Disease Clinical Research Network (ASID-CRN) members include the following: Royal Brisbane & Women’s Hospital: John McNamara and Rachel Sieler. The Alfred Hospital, Melbourne: Jill Garlick, Jess Costa, Janine Roney, and Nigel Pratt. American University of Beirut Medical Center, Lebanon: Houssam Tabaja, Joumana Kmeid, Ralph Tayyar, and Saeed El Zein. Dandeong Hospital, Australia: Stephanie Jones. Geelong Hospital, Australia: Raquel Cowan, Alex Tai, Belinda Lin, Babak Rad, Eleanor MacMorran, and James Pollard. Istanbul Medipol Mega Hospital Complex, Turkey: Rumeysa Dinleyici, Ayse Istanbullu, Bahadir Ceylan, and Ali Mert. King Fahad Specialist Hospital, Dammam, Saudi Arabia: Mai Hashhoush and Taleb Dalwi. Monash Medical Centre, Australia: Tony Korman, Rula Azzam, Michael Birrell, Carly Hughes, Sadid Khan, Jillian Lau, Layyang Lee, Karen Lim, Yi Dani Lin, David Lister, David New, Nastaran Rafiei, James Stewart, Alex Tai, Mohamad Ali Trad, and Victor Aye Yeung. Middlemore Hospital, Auckland, New Zealand: Stephen McBride, David Holland, Christopher Hopkins, Christopher Luey, Susan Taylor, and Susan Morpeth. Mater Hospital, Brisbane, Australia: Melissa Finney and Megan Martin. North Shore Hospital, Auckland, New Zealand: Umit Holland. National University Hospital, Singapore: Jaminah Ali and Roland Jureen. Princess Alexandria Hospital, Brisbane, Australia: Neil Underwood, Andrew Henderson, and Naomi Runnegar. Peter McCallum Cancer Centre, Melbourne, Australia: Monica Slavin. Royal Perth Hospital and Fiona Stanley Hospital: Owen Robinson. Sunnybrook Hospital, Toronto, Canada: Asgar Rishu. Wollongong Hospital, Australia: Samia Shawkat, Janaye Fish, Kwee Chin Liew, and Peter Newton. Santa Maria Misericordia Hospital, Udine, Italy: Maria Merelli, Alessia Carnelutti, Silvia Ussai, and Davide Pecori. Tan Tock Seng Hospital, Singapore: Ezlyn Izharuddin, Barnaby Young, and Ying Ding. Westmead Hospital, Sydney, Australia: Ristila Ram, June Kelly, and Neela Joshi. Charlotte Maxeke Johannesburg Academic Hospital, South Africa: Guy Richards, Oliver Smith, and Ahmad Alli. Groote Schuur Hospital, Cape Town, South Africa: Inge Vermeulen, Brenda Wright, Chedwin Grey, Annemie Stewart, Denasha Reddy, and Sean Wasserman. King Abdulaziz Medical City, Riyadh, Saudi Arabia: Hanie Richi, Khizra Sultana, Nouf Alanazi, and Eman Bin Awad. Ospedale Luigi Sacco, Milan, Italy: Fabio Franzetti. Pretoria Academic Hospital, South Africa: Anton Stolz, Elsabe De Kock, Tebogo Magongoa, Marizane Dutoit. “Sapienza” University, Rome, Italy: Alessandro Russo. San Remo Hospital: Chiara Dentone. Townsville Hospital, Australia: Damon Eisen, Liz Heyer.

Additional Contributions: We thank the data and safety monitoring board for its assistance with the study: Jesus Rodriguez-Baño (Infectious Diseases Division at Hospital Universitario Virgen Macarena, Seville, Spain) and Yohei Doi (Division of Infectious Diseases University of Pittsburgh, Pittsburgh, Pennsylvania), with independent statistical advice from Aaron Dane. Simon Forsyth, PhD (University of Queensland), helped manage the REDCap database. We also thank Henry Chambers MD, PhD (University of California, San Francisco), and Scott Evans, PhD (Harvard University), for their thoughtful review of the manuscript. Amy Jennison, PhD, and Rikki Graham, PhD (Forensic and Scientific Services Laboratory, Queensland), and the Australian Genome Research Facility helped facilitate bacterial whole-genome sequencing. Nouri Ben-Zakour, PhD (University of Sydney), and Mark Schembri, PhD (University of Queensland), also supported the genomic data analysis. Andrew Henderson, MBBS (University of Queensland), Ernest Tan (University of Queensland), and Kyra Cottrell, BAppSc (University of Queensland), assisted with phenotypic testing of the bacterial strains. Mark Chatfield, MSc (University of Queensland), helped attend to reviewers’ statistical comments. None of these individuals received compensation for their role in the study. The protocol was developed and endorsed by the ASID-CRN, with input from Jeffrey Lipman, MBBCh (University of Queensland), Jason Roberts, PhD (University of Queensland), Andrew Stewardson, MBBS, PhD (Monash University), Sanjoy Paul, PhD (University of Melbourne), and Emma McBryde, MBBS, PhD (James Cook University). They did not receive compensation. We thank the site investigators, collaborators, and research assistants for their help with the study, as well as the participating microbiology laboratories for their assistance with storing and shipping organisms.

I’ve been putting off writing about this topic for a while because we’re currently in a period of time where milk and dairy products are vilified foods. I’m a big proponent of the idea that ALL foods have pros and cons, and I think milk and dairy products have way more pros than cons. The inability to digest milk and dairy products is often due to additives, quality, and a person’s gut health and metabolic rate, rather than milk and dairy products being “bad foods.”

Thankfully, my intern, Nosheen Hayat, was up to the challenge! Nosheen is a dietetic intern at the National Institutes of Health and a Gates Millennium Scholar. She received her Masters of Public Health degree from the University of Michigan. I am grateful to her for tackling this tough, but timely blog post. Enjoy!

Many people (particularly in the vegan circles) make the argument that humans are the only mammals that drink another mammal’s milk and thus, it is an “unnatural” behavior. However, humans are also at the top of the food chain and the only mammals on earth that drive cars, cook their food, and use technology.

Dairy consumption has been a human practice for at least 8,000 years. In many cultures, milk is regarded as an important food and used to make butter, cheese, yogurt, and kefir.

Despite a long history of dairy being an integral component of the human diet, it has recently been vilified and alternatives such as almond, rice, and soy milk have become popular. One reason why dairy is considered an “unhealthy” food is due to its saturated fat content. Many publications since the 1950s have linked saturated fat with increased risk for heart disease; however, more recent publications are showing this may no longer be the case. Research now shows that saturated fat may not be associated with an increased incidence of cardiovascular events (1).

Milk consumption is associated with reduced risk for a number of diseases, including childhood obesity, type 2 diabetes, cardiovascular disease, stroke, colorectal cancer, bladder cancer, gastric cancer, and breast cancer; research also shows a positive effect on bone mineral density (2). While humans have been drinking milk for thousands of years, drinking plant-based milk is a new phenomenon and its consequences on health are yet unknown.

Not only is milk cheap and easily accessible for most individuals, it is also a rich source of magnesium, potassium, selenium, vitamins A, B, D, and K. It is a naturally balanced food—containing 87% water, 5% sugar (lactose), ~3.5% protein, and ~4% fat.

However, not all milk and dairy is created equal.

Grass-fed, Organic vs. Conventionally Farmed Milk

Grass-fed milk comes from cows that are allowed to graze on pasture for most of the year rather than being fed a processed diet (i.e. genetically-modified corn and soy). This method of farming creates an environment for happy, healthy cows. Grass-fed milk has a lower omega-6 to omega-3 ratio, which is important for good health and reducing inflammation in the body (3). It also has higher amounts of conjugated linoleic acids (CLA), which are associated with reduced risk for cardiovascular disease (3).

Purchasing organic milk can reduce the amount of pesticides in your milk and guarantee that the feed provided to the cows is not genetically modified. However, it does not imply that the cows your milk comes from are allowed to graze on pasture or be unconfined.

Conventionally farmed milk typically comes from cows that are fed a processed diet, consisting of soybean, corn, and other grains as well as antibiotics. Additionally, these cows are not allowed to graze on pasture and live in very unsanitary and stressful conditions.

Homogenization of Milk

The purpose of homogenization is to ensure that the fat or cream of the milk does not separate from the liquid. This is done by forcing the fat molecules through small holes or mesh at high pressure. One problem with homogenized milk includes the breakdown of casein micelles, which result in calcium phosphate soaps that can irritate the gut lining and decrease the bioavailability of calcium and phosphorus found in milk (4).

Homogenization can also introduce oxygen into the milk product, which can cause excess bloating and gas when it interacts with the bacteria in the gut of individuals with gastrointestinal issues. Lastly, homogenization can inactivate a protein called lactoferrin, which exhibits anti-bacterial properties by binding up iron and reducing its access to gut bacteria (5).

Opt for a non-homogenized milk, if possible. However, if you can’t get access to a non-homogenized milk, it’s no reason to avoid milk! Homogenized milk is still a great source of protein, minerals, and vitamins.

Pasteurization of Milk

When milk is pasteurized, it is heated to a specific temperature for a length of time and then cooled immediately. The temperatures and length of time vary based on type of pasteurization. Heat treatment is used to destroy potentially pathogenic bacteria; however, it can also inactive enzymes and reduce the percentage of nutrients found in milk.

Unpasteurized or raw milk is not heat-treated. However, raw milk is illegal in most states and difficult to find. If you live in a state that allows the sale of raw milk (i.e. California), it is important to visit the sourcing farm and see their practices to ensure cleanliness of their operations and proper care of their farm animals.

Low-pasteurized milk is heated in small batches at a lower temperature but longer period of time than regular pasteurized milk—to 145ºF for 30 minutes.

Regular pasteurized milk is heated to a temperature of 161ºF for about 15 seconds and then cooled immediately.

Ultra-pasteurized milk is heated to a minimum of 280ºF for at least two seconds. The higher temperatures kill more bacteria and ensure longer shelf-life of milk processed with ultra-pasteurization.

Pasteurization can reduce the amount of immune-modulating proteins in milk, such as lactoferrin; it can inactivate enzymes and reduce the amount of vitamin C, B6, iron, manganese, and copper (4). Ultra-pasteurization further reduces the vitamin and mineral content of the milk, cause formation of lactulose (a laxative) through lactose isomerization and Maillard reaction products, which can reduce the bioavailability of proteins and minerals in milk (4, 6).

While low pasteurization to no pasteurization is the best option, it can differ person to person depending on their digestive health. Individuals struggling with digestive issues may have symptoms of bloating, gas, and abdominal pain when drinking raw milk. These individuals may do better with a pasteurized or ultra-pasteurized milk product. Or vice versa, these same individuals may do better on raw milk or low-pasteurized milk. It is important for you to look out for symptoms after drinking milk to see if the type of milk you’re drinking is working for you.

Context of Drinking Milk

Now that we’ve discussed what to consider when purchasing milk, let’s talk about the different physiological contexts of drinking milk.

Many people cannot drink milk due to lactose intolerance, which occurs when not enough lactase (a digestive enzyme that breaks down the sugar lactose) is produced. Often times, a lack of lactase production is considered “unfixable,” however, underlying issues such as hypothyroidism or a low metabolic rate can be the root cause of a lactose intolerance. Digestive enzymes and stomach acid production decreases in a hypo-metabolic state, not only because the body is now in a stress response state and shunts resources away from the rest and digest system, but also because a slower metabolic rate requires less caloric intake and therefore, less inputs to the digestive system are needed (7).

Lactose intolerance can also present itself as a symptom of underlying gastrointestinal issues, such as small intestinal bacterial overgrowth (SIBO) or irritable bowel syndrome (IBS) (8). Microbiota dysbiosis usually occurs when there is an imbalance in the number of good to bad bacteria. Good bacteria thrive off of sugars and produce useful byproducts, such as acetic acid and butyric acid, which are subsequently absorbed into the bloodstream or used to activate thyroid hormone in the gastrointestinal tract. However, bad bacteria produce an excess amount of gas, which presents itself as flatulence and bloating, when they have access to sugar molecules (i.e. dairy sugar lactose, a disaccharide). And they subsequently suppress the growth of good bacteria by reducing their access to nutrients as well as over-proliferating.

For individuals who may struggle with gastrointestinal issues, you can reduce the likelihood of bloating, gas, and pain with drinking milk by opting for warm over cold milk. The optimal temperature for digestive enzymes is 98.6 degrees. When we drink cold milk, we reduce the temperature of our digestive tract and reduce the effectiveness of enzymes responsible for digesting our food.

It’s also important to note that individuals who have lower metabolic rates are likely unable to convert the amino acid tryptophan in milk to a B vitamin called niacin. In individuals with high metabolic rate, tryptophan is easily converted to niacin, which is used to break down carbohydrates, protein, and fats from our meals, support liver and digestive function, and much more (9). Eating a balanced meal prior to drinking milk ensures that the tryptophan in milk is converted to niacin, as opposed to the stress hormones serotonin and melatonin (10).

Milk is a balanced food with many nutrients that can be used to support good health. For people with low metabolic rate and gastrointestinal issues, it can be difficult to consume milk. Addressing the metabolic rate and GI issues almost always results in better digestibility of milk and therefore, increased access to a great source of nutrients.

Cheese

Cheese, like milk, is a great source of nutrients. However, the problem with cheese is the excess ingredients manufacturers add to them, such as whey protein, gums, carrageenan, enzymes, GMO cultures, food coloring, and “natural” or artificial flavoring. These additives can make it difficult to digest the cheese products, which is why it’s important to look for a cheese with the least number of ingredients (9).

For example, when searching for organic ricotta cheese, look for a brand that only has skim milk, salt, and vinegar on the ingredients list. Also, look for cheeses that have animal rennet as opposed to enzymes or other types of rennet, which can be allergenic. Many European imports still make cheese the traditional way with animal rennet.

Yogurt

Individuals who struggle with hypoglycemia, a sluggish liver, or are hypo-metabolic should eat yogurt (and other fermented foods) in small quantities. Lactic acid from yogurt, when absorbed, can cause a stressful response in the body by forcing the liver to use its glycogen stores for energy to convert the lactic acid into glucose.

When consuming yogurt, choose a low-fat Greek option, which will be lower in lactic acid (because it has been strained); will have less additives; and more calcium and protein.

References

1. https://www.ncbi.nlm.nih.gov/pubmed/29628045 (see also: https://www.ncbi.nlm.nih.gov/pubmed/26268692, https://www.ncbi.nlm.nih.gov/pubmed/20071648)
2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5122229/
3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5980250/
4. https://www.sciencedirect.com/science/article/abs/pii/S0924224406000550
5. https://www.ncbi.nlm.nih.gov/pubmed/18573312
6. https://www.hindawi.com/journals/ijfs/2015/526762/
7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2699000/pdf/WJG-15-2834.pdf
8. https://www.ncbi.nlm.nih.gov/pubmed/26393648
9. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3729278/
10. “Fuck Portion Control” by Nathan Guy Hatch
11. “How to Heal Your Metabolism” by Kate Deering

Could a change in diet be beneficial to people with autoimmune diseases such as lupus? A Yale-led team of researchers have revealed how a dietary intervention can help prevent the development of this autoimmune disease in susceptible mice. The study was published in Cell Host & Microbe.