Christoph Nabholz: Moderated discussion and Q&A on individual health

Christoph Nabholz: Moderated discussion and Q&A on individual health


We wanted to quickly discuss here on stage
as well. We’ve just looked into this personalized nutrition,
and I think there is a big field open out there which is about consumer nutrigenetics,
and I think that industry has picked up on that and is selling it to market. Last year is probably the year of the nutrigenetics,
coming to mark direct consumer testing and sales have been going through the roof. What are your reactions to that development? In a word rubbish. The genetics of response to food, and whether
you’re gonna be this kind of person, or this kind of person is based on statistical results
from genes that are in terms of P value correct, there is a significant difference between
the groups, but for an individual it is barely different to tossing a coin, so he variants
explained by genetics … We look at it … We’ve talked about obesity, yes there a high, over
100 genes found for obesity, but they explain 1% of the variants between people. This is what we are talking about and you
got companies doing this testing saying, “Well if you’ve got these genes, you’re more likely
to do X and Y.” It’s a con basically, but it’s statistically
correct, so they are proposing has slanted validity, but as an individual none. There’s two exceptions for that. I think one is lactose intolerance, the lactase
gene is actually quite a reasonable one to measure, and has a decent prevalence so you
will gain something for that, although may with the gene can still drink milk. It isn’t absolute. Similarly with alcohol dehydrogenase, whether
you are a fast converter or not, you’re slightly more likely, but generally more people know
that, so it’s not a big deal. So the rest of it unfortunately is smoke and
mirrors. Okay, José you’ve been talking about how
to deliver this personalized message. Genetics, Genomics is part of it. I guess the belief behind it is that you gie
them something ultimate right? It is your genome that is different and that’s
why you have to adopt to a new nutritional profile. Whether we go to the DTC mark, or maybe more
sort of a clinical process where we go more in depth analysis of say epigenetic analysis
or so on expression profiling could be part of it. As you see this is really a motivating factor
people to actually then adhere to this new nutritional guidance that they are getting? Well first although I would not put it in
such simple word as rubbish, I agree in general with what Tim was saying about what are benefits
of the current offerings, right? In terms of the market. We just don’t have the ability to provide
that personalization, and that’s what I tried to illustrate in one of my last slides in
which yeah can … It’s statistically significant, right? But when it comes to that offering of “Oh
we can really provide you with a precise kind of diet that you need.” It depends on where you are in that cloud
of points that we have there. We thought, and there is some evidence to
suggest that one of the reasons why the global recommendations are not working not because
they are bad, it’s because people don’t follow them. They don’t adhere to them.We thought that
by providing individual with that incentive of the personalization, right? Because people look for that customization
that people will be following those, will get more benefit out of recommendations that
are just proven recommendations. There is some evidence to suggest that … Is it like a placebo effect? Precisely … You give people some false reason to follow
something, and then they will. Right but I mean even of it’s a placebo effect,
it’s good because we achieve our full purpose. All for placebo. Right. But there comes a point where people are paying
a lot for a placebo effect that may not be worthwhile. Okay, it’s good with synthesizing the … We
use one word to synthesize. However, based on for example the food for
me, in which you can’t see any major advantage of using the additional genetic information
in terms of changing the lifestyle, or the dietary habits of the individuals, that puts
also some kind of gray area to this placebo effect. Now, in thinking about that precisely this
morning and say, “Okay, people didn’t change their meat intake, or adhere to the healthy
recommendations more by knowing their genetics however, there is something that probably
you haven’t test, are they benefiting more than the people that don’t have the genetic
marker?” We don’t know, and probably you will say that
… We haven’t tested. These general guidelines are just … There
are so many guidelines out there. Which guidelines should we follow, right? I like actually Tim your approach where you
actually in and say well and go in a deeper understanding, and actually what are the changes
that we produce through these guidelines in our metabolic footprinting, right? Or in our microbiome diversity, right? That’s actually a better approach, because
then you can measure something then you can prove point actually what the guidelines are
bringing to you. If you are looking into that, and say like
guidelines on skipping the snacks for example, right? That’s something that we said should we do
that? Do we have the evidence? Can we prove that skipping the snacks is changing
the diversity of our microbiome, and we have actually now a marker to prove that? Many governments guidelines, including of
the UK, say that you should never skip meals. It’s written there in the guidelines, and
it keeps getting every year, it’s very bad, particularly skipping breakfast. The British like breakfast, the only meal
they can cook well, so they like to state down too, so they say, never skip breakfast,
it’s deadly, you’ll get fat. But there are five randomized controlled trials,
showing that actually if you keep the calories the same and you have less meals in a day,
and you skip breakfast, you’ll either keep the same weight or lose weight. So the opposite is actually true, but the
guideline still maintain, and I think it’s a big battle to stop this idea a few … I think it was about 20 years ago we suddenly
said, grazing is better than gorging, and it was all based on some very short term metabolic
studies showing changes in insulin and things like this. No long term studies at all and the microbiome
work suggests that is bad. We do need long periods of fasting, where
the microbes can regenerate the body, a whole different team of microbes comes out at night,
starts nibbling away at your gut lining, they eat that. This is the Akkermancia that also seems to
keep you thin. This feeds off the gut lining, tidies it up,
helps the immune system. I think as well as just gaining weight, there
is also gut health in there. I think this is a big change, and we’ve discussed
yesterday how snacking might actually be one of the big common factors in many of the bad
performing countries, and I think there now a bit more of a rationale for really changing
that. It was quite striking to see actually that
some of the microbiome that we looked at actually stood out as being protective right? Christian Sinella is one of these right? Do you fear that there is an industry out
there that is jumping on that and saying. “Wow this is the next Pill” And the Pharmaceutical
industry is gonna jump on that as the new obesity advisor, and just to take the pill
and it’s gonna fix your problem? Because it’s the right microbiome that we
are giving you? What’s interesting is in vast majority of
cases, we found that microbes rather than we think of them as causing disease, are protective. That’s why this idea of the more you’ve got,
the more likely you are to keep a stable health state. Many have multiple protective functions against
inflammation, et cetera. So it’s like the opposite of all our other
epidemiology where we are trying to find a cause, we actually looking in the opposite,
and for these obese protective microbes there are food companies now trying to put into
yogurt, putting it on to your cornflakes to get it to work, but anaerobes, they’re very
difficult to grow on their own and we might need to have them in communities. They often work in conjunction with other
microbes. I think industry is working on this, but it’s
still got a long way to go before these perfect pills can go. But Akkermancia we mentioned, just within
a year of some Mouse studies showing, they can help reduce obesity, there is a study
now going on in Belgium having Akkermancia as a probiotic on overweight diabetics. The speed of which you can actually test these
things is really refreshing, and because they are generally safe it’s a whole new era. You don’t have to wait 10 or 20 years for
Pharma, you can get on and actually do this. Last question to you José, before we open
the floor, genetic risk scoring you talked a bit about right? We have over 300 genes associated with type
two diabetes and studies show small incremental changes, are we gonna
look for this new … Because all of the data evidence is now coming together, we’ve got
the microbiome, we get the metabolome, and we can now all of a sudden bring this huge
risk score forward that is going to give us the right risk profile, and also the right
measurable to actually change and actually measure our outcome again. How quickly is this gonna happen? How far are we away from this super risk score
that we are all waiting for? Well every time that I get the question, it
doesn’t matter if it happens in the 90’s or in the early … I always play it safe, and
say “Okay, in the next five years, we will have that.” That number has not changed in the last 20
years. Obviously we have the … At least for the
genetic risk score, I don’t know if you agree with that. We have that in our hands, right? Whether it is for obesity, or for cardio vascular
disease diabetes … It’s not getting that much better. Precisely, I mean we have as we show here today, we have arrived to the bottom of the bar graph, when it comes to
extract genetic information. We can go from the genes to
the whole genome sequencing, and my suspicion is that we are not going to get much better
than what we have now. So we are at the point in which we could use
that information to predict future risk of disease. And it’s important to say future risk of disease
as something new than in the real world may not know, because things like what you indicated
before, which is lactose intolerance, right? Or alcohol response, people know that. Or coffee, coffee is another example. We can predict what people already know whether
coffee is going to alter your sleeping or not. I think we are at the point in which we could
use information that we have to predict risk. Excellent. Now to modulate the risk, we have some examples
using the combining the genetic risk score, with that information we can modulate that
risk, but again there is is much variability within each group that calling that precision,
nutrition is a little bit hard. Thank you. Good. Questions? Wow. A lot of questions so let’s take the first
person in the back there with that tie, good. Thank you. Thank you very much, my name is Richard Black,
Quadrant D consulting in Turfs University School in Nutrition Science and Policy. It’s a question of practicality for both,
differently though, and that is 25 years in the food industry, I always trying to reduce
things to practice. Doctor Spector, you were flagging the microbiome
and drug testing. Who’s microbiome should we test the drug against,
and at what time of the day? Because until you said it in the comments
now, it fluctuates through out the day the different populations. I don’t know … It’s a wonderful goal, I
don’t know we’d actually execute against that. And for Doctor Ordovas, on the personalized
nutrition, we can’t get people to follow basic guidelines now. There is probably 50% of the population is
not even interested in following guidance, no matter how personalized. I see the value, absolutely see the value,
but reducing it to practice strikes me as almost insurmountable. I’d just like to hear your views on both of
those. Thanks a lot for that question. Should drug testing involve the gut microbiome? If we see it as an organ that we’ve just now
been able to test was always there. They do drug safety testing for the liver,
the kidneys the pancreas, the brain, so yes you should include it as an extra organ, collect
store samples beginning an end, do meta genomic analysis which is not expensive and add it
to that portfolio of any drug, and if there is a detrimental effect in terms of reducing
diversity, or increasing pathogenic species, report it. That’s just common sense. I think if people did that then you wouldn’t
have this idea that only 10 years after everyone is on a PPI do you suddenly realize there
are side effects, and people are getting extra C.Diff infections, and they are having other
minor problems of the bowel, et cetera that people didn’t know, because the GP’s are saying,
“This is virtually a risk free drug.” Because just no one had looked at it. And the same with opiates, and all those other
drugs, so it should be standard, and I think in the same way that all drug companies now
take some DNA samples to see of there is a particular genetic variant that has a bad
side effect, the same should be true for Pharmaceuticals. Okay in terms- And third I should say in the food manufacturers,
I think how they process foods at the moment is just you give a thousand times to a Rat
and see if it’s liver explodes, and it’s yes or no. That hasn’t changed for 50 years. We need to move on with our safety standards,
and actually start saying the effects of all these cumulative chemicals, what do they have
on the average human microbiome? You take a hundred people, and that would
give you a snapshot of what’s going on. José? Very brief because we have analyzed that previously
in terms of the practicality. It’s not feasible nowadays to apply that to
the population at large, but obviously it’s early adapters that are going to go after
this, and hopefully we are going to learn from them whether this is going to work or
not. Good, next question. Jenny Brand Miller. I’m a little bit of skeptic that genetic differences
will make a difference to the diet, that is healthiest for us. I say that on the basis that, at the moment
the biggest genetic differences between us, is whether we have an X chromosome, two X
chromosomes, or an X and Y. A huge difference, a whole chromosome and
yet to my knowledge nobody’s worked out that there is a good diet for females, and a good
diet for males. Well let me … I am sure you have something
to say about that Yeah very briefly, at least from the statistical
perspective, we have identified some genes that the gene diet interaction works for women,
and it doesn’t work for men, and vice versa. So based on the genetic we could aim for some
kind of personalization based on gender. However, this is in theory we have not taken
that to the practical test. But the similarities actually outweigh the
differences, so in terms of most the genetic scores and just the risk factors for most
of the diet related phenotypes, there is very little difference between the sexes, and in
a microbiome, they’re also very little differences interestingly between the sexes. It may not be as large as we think. Okay. Good, next question we take from in the back
there. Let’s try that, good. Hello, Sam Robson from Aberdeen. What does the panel think about the impact
of circadian rhythms and time restricted feeding, or intermittent fasting on an individuals’
response to food? Well that’s something that we have been studying
for the last few years, the influence and it has been mentioned in our previous question
… The influence of the circadian rhythms, for example we have studies in which for people
trying to lose weight, depending on the time of the day that you have your meals, they
will respond better or worse to the weight loss program, after adjusting for the calories
consumed by the individuals through the day. Time of the day is something important. We have investigated with the various genetic
factors involved in this effect, and for example we’ve found that Perilipin-1 gene, which is
the gene calling for the major protein in the fat droplet in the lipocyte,
is at least a statistically significant different between those that are affected by the time
of the day which eat, and they are the ones that are not affected. Personally I believe a lot in that chronobiology
component of our health, and in addition to providing information about what people should
be eating, we should also try to get better knowledge about when the food should be consumed. Tim Intermittent fasting? Microbes do have a circadian rhythm as well
as humans, and they tend to fit into a 24 hour clock as well. When shift workers are tested they tend to
have abnormal microbiomes, and they produce abnormal metabolites, when that system is
stressed and goes out of sync. It explains and that’s also the same with
people with sleep disturbances. And we know that sleep disturbances are associated
with increased obesity as well so it’s probably the microbiome is upset therefore, many of
the metabolites in the blood in the microbiome actually supplies perhaps 30% to 40% of the
metabolites in the blood, start going away. The other question was on intermittent fasting. There isn’t that much data in the microbiome
on that, but certainly fasting periods … Doesn’t seem to matter whether it’s twice a week,
or it’s everyday for a little bit, do seem to be generally beneficial in improving the
diversity of the microbiome. The data isn’t perfect but it’s looking like
the greater the fasting periods if they are not too large is beneficial and continuous
eating, doesn’t allow the microbes time to recover and do their repair job. Last question in the back. Thank you my name is Hannah, I’m in food development. Can I ask Tim, I’m a big fan of fiber and
fats, could you tell me what your views are about inulin and whether or not it really
is a beneficial fiber, or just a lot of hype, thanks. Inulin is the one that has been studied most,
so most of the data on fiber certainly from food industry about additives has been through
inulin, and so most of the benefits have been shown through it. Now there is a lot of other fibers we haven’t
properly studied, many of them we still think of fiber as one particular chemical, where
it actually it’s hundreds of different combinations. I don’t think we fully know, one question
I do get asked is, is chemical inulin as good as having a Jerusalem Artichoke or a Sun choke,
which is full of it or Chicory, and my answer is no. I think you need a variety of fibers to have
a variety of results, and the more diverse the better. I don’t think we’re gonna replace all our
natural fiber with just a few spoonfuls of Inulin. I think that would be a big mistake, it’s
like going down the Omega-3 supplement route rather than having a rich source of Omega-3’s. Good we are at the end of this conversation. Next step is we have a break, so we can enjoy
that. But before we go there just to declare myself,
sorry I haven’t done that. I’m working for Swiss Re, that’s my bias. All I’m biased to is that we would like to
do something good for everyone, and that everyone is more healthy then … And what the health
outcome is, and how we generate the healthy outcome we don’t matter, but food seems to
be a really important matter here in that case, so that great. My taste is on chocolate, I love chocolate,
and otherwise I eat everything. I try not to eat too much, but that’s all
I can to that. Many thanks Tim and José. You can also meet them later on. Thank you.

Leave a Reply

Your email address will not be published. Required fields are marked *