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Ethnic differences in the prevalence of obesity occur, majorly in part due to differences in the rates of metabolic syndrome (which is actually a few variables including high blood pressure, high blood sugar which leads to insulin resistance, excess visceral fat around the waist which is the ‘skinny fat‘ phenomenon, and abnormal blood pressure levels) and obesity. Ethnic differences in these variables do, in part, show how the three ethnies differ in rates of obesity. I will discuss the differences between each ethny in regards to metabolic syndrome and sleep and how it leads to the differences in ethnic obesity rates.
There is a ‘missing hour of sleep‘ when comparing blacks and whites. On average, blacks get 6.05 hours of sleep while whites get 6.85 hours of sleep. Of course, the same old racism argument comes up, which, if one ‘percieves’ discrimination, I wouldn’t doubt that it would have an effect on sleep due to a rise in cortisol, which affects sleep due to the raised levels making you restless and not able to fall asleep. Insulin levels then rise due to the rise in cortisol, which is the cause of obesity.
Some studies may try to say that racism and other forms of discrimination are a factor, without even thinking of genetic factors. Another study that Frost cites says that duration of deep sleep and duration of stage 2 (light sleep) is correlated correlated in African Americans with perceived discrimination. The authors defined ‘perceived discrimination’ as the extent to which one believes that their ethnic group have been discriminated against by society. Still even when controlling for discrimination, there were still marked differences between blacks and whites and how long they slept.
Frost then talks about how sleep patterns are heritable and cites studies done on Africans in Africa. One study found that there was an hour sleep difference between Ghanaians and Norwegians on the week days and between a quarter to half hour less on weekends. He shows another study showing that Nigerian college students sleep 6.2 hours a day while getting 70-minute naps in the afternoon.
Frost concludes that the African sleep patterns is normal on Africa. Africans are more active during the cooler times of the day and sleep during the bitter periods. Frost says those who evolved in more northerly climes are particularly adapted to a certain sleep pattern with the same holding true for Africans.
However, these sleep patterns in first world countries have negative effects on metabolism and rates of obesity.
Here are some more studies showing that blacks sleep less than whites:
The sleep of African Americans: a comparative review: The researchers found that blacks take longer to fall asleep than whites, report poorer sleep quality, have more light and less deep sleep, and nap more often and longer. This is a huge recipe for risk factors for obesity, and it shows in their demographics.
Unfair Treatment is associated with Poor Sleep in African American and Caucasian Adults: Pittsburgh SleepSCORE Project: This is one of the studies spoken about above that show that discrimination leads to less sleep. Though, it holds for both black and white adults. The researchers conclude:
Taken together, the confluence of perceived unfair treatment as a chronic stressor and poor sleep and the interplay between the two may have critical roles in long-term health problems.
African Genetic Ancestry is Associated with Sleep Depth in Older African Americans: The researchers hypothesized that “racial differences in sleep phenotypes would show an association with objectively measured individual genetic ancestry in AAs.” They conclude that the slow wave sleep may have genetic underpinnings.
Mexican Americans sleep less than do Mexican immigrants. US-born Mexicans are 40 percent more likely to be short sleepers. This is attenuated by environmental factors such as smoking and stress, which shorten the duration of sleep (smoking decreases the Body Set Weight, whereas cortisol along with insulin in tandem increase it).
Also, in this study by Roane et al (2014) looked at the link between sleep disturbances and stress in Mexican Americans (average age 55) and non-‘Hispanic’ whites (average age 66). Mexicans reported higher levels of sleep disturbance (25 percent) compared to whites (17 percent). They conclude that disturbed sleep was positively correlated with depression.
So both blacks and Mexicans sleep less than whites. These differences in sleep between these three ethnies also affect the prevalence of obesity in these populations.
Obesity and Sleep
It’s long been known that poor sleep habits make people fat. This is due to the effects of insulin and cortisol. Increased insulin comes before increased cortisol–increased insulin is the cause for obesity. Sleeping less is linked to obesity. Since, as described above, the three ethnies differ in sleep patterns, the same also holds true for obesity rates (Ogden at al, 2014). The trends are as follows: 67.3% for whites, 75.6% for blacks, and 77.9% for Hispanics. Though, sleep is only one factor involved with obesity.
Getting adequate sleep is extremely important. Not doing so can lead to a myriad of negative health implications:
Sleep is an important modulator of neuroendocrine function and glucose metabolism and sleep loss has been shown to result in metabolic and endocrine alterations, including decreased glucose tolerance, decreased insulin sensitivity, increased evening concentrations of cortisol, increased levels of ghrelin, decreased levels of leptin, and increased hunger and appetite. Recent epidemiological and laboratory evidence confirm previous findings of an association between sleep loss and increased risk of obesity.
So a lack of sleep leads to an increase in ghrelin levels, decreased levels of leptin (the same effects as caloric restriction over time), increased appetite and hunger, increased evening cortisol (which insulin spikes then follow), decreased insulin sensitivity (the cortisol brings it back up and most people are insulin resistant independent of diet), decreased glucose tolerance, etc. We can see that these ethnic differences in sleep, which are partly genetic in nature, can and would have great effects on metabolism, contributing to the ethnic differences in obesity rates.
And from Harvard:
For example, in the Nurses’ Health Study, researchers followed roughly 60,000 women for 16 years, asking them about their weight, sleep habits, diet, and other aspects of their lifestyle. (2) At the start of the study, all of the women were healthy, and none were obese; 16 years later,women who slept 5 hours or less per night had a 15 percent higher risk of becoming obese, compared to women who slept 7 hours per night. Short sleepers also had 30 percent higher risk of gaining 30 pounds over the course of the study, compared to women who got 7 hours of sleep per night.
Damn!! This, pretty much, mirrors the black-white difference. I’d love to see a racial breakdown of this cohort and will keep an eye out for one, but in the meantime, those who were short sleepers had a 30 percent higher risk of gaining 30 pounds over the course of the study in comparison to women who got 7 hours of sleep per night. Blacks are the most likely group to be overweight and obese in the US, and this data from the Nurses Health Study (which tons of data can be drawn from this study) shows one reason why, however the driver is cortisol > insulin > processed carbs > increased insulin > insulin resistance > increased insulin > vicious cycle > obesity. These differences in sleep almost perfectly mirror the ethnic differences in obesity.
There are several possible ways that sleep deprivation could increase the chances of becoming obese. (1) Sleep-deprived people may be too tired to exercise, decreasing the “calories burned” side of the weight-change equation. Or people who don’t get enough sleep may take in more calories than those who do, simply because they are awake longer and have more opportunities to eat; lack of sleep also disrupts the balance of key hormones that control appetite, so sleep-deprived people may be hungrier than those who get enough rest each night.
Ah the old ‘exercise to increase the Calories Out part of the equation’. however, Calories Out does not stay constant. This also rebuts the ‘Eat Less and Move More’ CICO (Calories In/Calories Out) model of obesity, showing that because it doesn’t take insulin into account, it’s doomed to fail.
Speaking of insulin, it’s about time I focused on metabolic syndrome.
As I discussed in a previous post, Race, Obesity, Poverty, and IQ, metabolic differences exist between race/ethnicity. ‘Hispanics’ metabolize carbohydrates differently, blacks have a lower fiber intake (increased fiber protects against obesity, another correlate) while whites have a more high fat diet. Contrary to popular belief, dietary fat doesn’t make you fat as it’s the macro that spikes your insulin the least.
Diaz et al (2005) showed that minority populations are more likely to be affected by diabetes mellitus which may be due to less healthy diets and/or genetic factors. Using the National Health and Nutrition Survey for 1999-2000, they analyzed overweight, healthy adults, calculating dietary intake variables and insulin sensitivity by ethnicity. They characterized insulin resistance with fasted insulin, as those who are more likely to become insulin resistant have higher fasted insulin levels (levels taken after waking, with the subject being told not to eat the night before as to get a better reading of fasted insulin levels). Non-‘Hispanic’ whites had higher energy and fat intake while ‘Hispanics’ had higher carb intake with blacks having lower fiber intake. Blacks and ‘Hispanics’ were more likely to have lower insulin sensitivity. However, ‘Hispanics’ were more likely to have lower insulin sensitivity even after controlling for diet, showing that metabolic differences exist between ethnicities that affect carbohydrate metabolism which leads to higher rates of diabetes in those populations.
In ‘Hispanics’, several loci were discovered that play a role in hepatic (relating to the liver) fat content. Along with showing that ‘Hispanics’ have lower insulin (which due to low insulin, blood glucose builds up in the blood stream leading to diabetes) and showing that they metabolize glucose in the liver differently due to differing loci leading to more cases of fatty liver, this shows how and why ‘Hispanics’ have higher rates of Type II Diabetes Mellitus (TIIDM).
Since TIIDM affects Mexican Americans more, better measures to address their differences in carbohydrate metabolism need to be taken. Racial and ethnic differences in TIIDM are as follows:
7.6% of non-Hispanic whites
9.0% of Asian Americans
12.8% of Hispanics
13.2% of non-Hispanic blacks
15.9% of American Indians/Alaskan Natives
Whites eat a higher fat diet, which means a decrease in carbs. Asians eat white rice which spikes blood glucose eliciting a high insulin response leading to TIIDM, ‘Hispanics’, non-‘Hispanic’ blacks, and Indians and Alaskan Natives (I wish they separated Indians and Alaskan Natives as I’m almost positive that Alaskan natives have a lower rate) all eat high carb, low fat, low protein diets. Carbohydrates are a main staple, and since they spike insulin the most, they are the cause for obesity and TIIDM rates in these populations.
Turning my attention over to metabolic syndrome and blacks and whites, we can see that black women with PCOS have an increased risk for cardiovascular disease and metabolic syndrome in comparison to white women with PCOS. The researchers say that after controlling for age and body mass index (BMI) “black women with PCOS had a significantly increased prevalence of low high-density lipoprotein and high glucose. The general CVD risk was significantly increased in black adults with PCOS.” Though, a longitudinal study needs to be carried out to assess the independent impact of race and PCOS with CVD (Cardiovascular Disease).
Blacks have a higher chance to be diagnosed with metabolic syndrome since they are also at increased risk to have elevated blood pressure (hypertension), become obese, and be diabetic. This is due to their diet, which is due to their low IQ (obesity is correlated with intelligence), and different metabolism in comparison to whites.
There are also metabolic differences between race and sex. Fat oxidation is lower in black than white men and in African American men/women and white men/women, they have a lower metabolic rate!!! 24-hour energy expenditure is lower in black women in comparison to white women, whereas physical activity energy expenditure (PAEE) is the same as whites. Contrasted with women, black men had higher PAEE than white men. The authors conclude:
In conclusion, this comparative study of 24-h energy metabolism in African Americans and whites with use of a respiratory chamber not only confirms the previous findings from ventilated-hood studies of a lower resting metabolic rate, but also suggests a lower 24EE in African American women than in white women. Although only marginal ethnic differences in metabolic rate were found in men, African American men seem to have a lower rate of fat oxidation than do white men. The underlying mechanisms for these sex differences and the significance of these findings with respect to the development and maintenance of obesity remains to be investigated in longitudinal studies.
Metabolic Syndrome and Obesity
I’ve been in a few discussion with PumpkinPerson on phenotype and if the similar phenotype found in Australoids and Pacific Islanders meant they were Negroid. However, just because two *dissimilar groups* look *phenotypically similar*, that doesn’t mean that they are *genotypically similar*. Afrocentrists have also latched on to this ridiculous theory, saying that blacks are ‘all over the world, displaced by whites yada yada yada’. Today, I’ll show that just because those two groups look similar to Africans doesn’t mean that they are similar on the genotype.
PP wrote an article last week, The importance of leaving Africa, which I will be quoting from for the remainder of this article.
The root of this debate is not so much genuine scientific disagreement, but ethnic genetic interests. The black Afrocentrists believe it’s good for black people to be seen as part of this larger, global black community, thus dispelling the claim that blacks only left Africa in chains. For leaving Africa was one of the milestones that separates humans from our closest living relatives (chimpanzees), so the claim that blacks never left Africa is seen as racist indeed.
I agree here that Ethnic Genetic Interests is the main driver of the dispute.
But if the mere leaving of Africa did indeed screen for IQ, why do the Australoids score even lower on IQ tests than sub-Saharan Africans do, and have somewhat smaller brains
Because the environment is similar it would select for similar phenotypes, but just because the environment is extremely similar doesn’t mean that no genetic change occurred in the 70 ky that Australoids left Africa in.
By contrast, the non-black HBDers think it elevates their racial status to promote the idea that their ancestors did something that blacks couldn’t accomplish: leaving Africa.
Well, as I’ve covered here last year (time flys), those who left Africa had specific alleles, the DRD7 and DRD4 alleles, which are absent from SSA populations. This ‘wanderlust’, due to the DRD7 allele, is the *cause* of the migration OoA. It has nothing to do with being more intelligent than those who stayed, it has to do with the genetic mutation that arose from a common ancestor around the time of the OoA migration. The cause of the migration does come down to genetic differences in the founder population (s), but not intelligence differences.
Two notes on the DRD4 allele: populations with a history of migration have a higher chance of having the allele in comparison to sedentary populations. And: a correlation of .85 was found between km traveled and the rate of DRDR4 allele frequency distributions. These alleles are more prevalent in South America, which is not surprising since they had to travel the furthest.
PP then starts talking about why Australoids have lower IQs, saying:
With agriculture/civilization, the dark caucasoids traveled the World, spreading their high IQ mutation to every corner of the globe except those that are most isolated. So the mean genetic IQ of the entire World increased by 13 points, with the exception of places that were too hard to get to, such as Australia and Papua New Guineas, the Congo rain forest, the Southern tip of Africa, and the Americas. Since most of sub-Saharan Africa got the genes, they suddenly leaped from having lower IQs than the Austaloids, to being smarter (only the bushmen and pygmies, who like the Australoids, were too isolated to get the genes, remained behind the Australoids).
This is a great hypothesis. It makes a lot of sense. The ‘Dark Caucasoids’ as PP calls them, better known as Anatolian/Neolithic Farmers could have had a higher chance for more high IQ mutations due to the fact that they could farm and thus have a higher population giving more of a chance for higher IQs.
The downfall for the dark caucasoids was spreading these genes to whites and East Asians. Because of cold winters, East Asians and whites were smarter than pre-mutation dark caucasoids, and now with these mutations, they were smarter once again.
I’m confused here. What we call whites today did not exist that far back in the past. Europeans are an amalgamation of four different ancient populations, basically are an amalgamation of ‘Dark Caucasoids’. Is he also saying that the Neolithic Farmers were more intelligent than East Asians?
Eurasians didn’t become a distinct breeding group until the end of the last Glacial Maximum. This is why there is ‘genetic similarity’ to modern-day Europeans with some old, 10k year plus peoples in the Americas. Because the two groups didn’t split into distinct populations, they show a similar genotype. This is what proponents of the Solutrean Hypothesis need to get through their heads. (I recently got into a nice discussion over at The Alternative Hypothesis, scroll down for comments. I’m going to make a more comprehensive post on the SH in the near future as I have come across even better data on it.)
We can see from this PCA graph (from Zainel Abidin et al) that Australoids don’t even cluster in the vicinity of Africans. They are on the complete other side of the graph, showing how great of a genetic distance there is between these two populations. You can see the other Oceanic peoples (the orange dots, who Afrocentrists and others say are Negroid, Abos, Papuans, Melanesians, etc) are also clustered away from Africans. PCA graphs show that the three populations are not genetically similar and that phenotype, sometimes, isn’t enough to show who belongs to what racial grouping. PCA analysis refutes peoples ‘feelz’ on what they believe with their eyes. Even with this data, their ‘feelz’ still overrides the truth and they still believe lies.
While on this subject of similar phenotype not meaning one population is racially the same as another, people use this same fallacious reasoning for ‘white-looking’ peoples in the ME.
Quoting Razib Khan:
The final issue is that a lot of the phenotypes that we racially code are recent. This probably explains why groups like the Kalash and Nuristanis can look more like Europeans than South Asians, but they’re genetically more like South Asians.
What does any of this have to do with non-scientific things? I don’t really know. My interest in population structure is intellectual, not personal. But a certain type of person should probably stop talking about how white people have been in Europe for 40,000 years. First, the ancestors of modern Europeans 40,000 years ago were almost all residing outside of Europe. An assertion that holds until 15,000 years ago. And most would still be resident outside of Europe 8,000 years ago as depending on how you count/calculate. *** And, perhaps more importantly, the typical phenotype of Northern Europeans probably really coalesced only around ~5,000 years ago. ***
How can there be such phenotypic similarity in two populations separated by thousands of miles?
Easy. The Kalash and other ME ‘white-looking’ populations have ancient Siberian ancestry. As shown in my linked article, modern-day Europeans have a great deal of Siberian ancestry, mostly from the true Aryans, the Yamnaya peoples.
And in the comments Razib was asked:
“Could I bother you to list the top three theories/positions that you see falling into this unsupportable category?”
To which he responded:
“that phylogeny and phenotype track closely. just because you can’t tell the physical difference between two pops (e.g., solomon islanders and sub-saharan africans) they must be phylogenetically close. this is not the case.”
Pretty much seals the deal.
Just because populations look similar on the outside doesn’t mean they are genetically similar. As shown from Razib’s post, the phenotypes that we code are relatively recent, which is why there are some populations separated by thousands of miles yet look extremely similar.
This was said in the comments:
I can’t really tell about the genetics since I don’t have the scientific background, but my impression is a lot of those white identity guys have an extremely mythologised view of the past. This seems to be true even of the smarter ones; e.g. I recently read a bit of Richard Spencer’s twitter account (out of interest in the alt right phenomenon) and he throws out such totally retarded comments as “Europe has always been unified, even before Christianity” (totally ignoring what is known about the ancient Greeks’ intimate links to the Near East, the Greeks’ and Romans’ unflattering view of the northern barbarians, the emergence of Latin Christendom in the middle ages and the fairly late rise of the concept of Europe etc.) or “Europe is a nation”. There seems to be little awareness of the complexities of historical change because everything is reduced to some supposedly unchanging racial essence reaching back into the mists of prehistoric times. Now I’m pretty far right and “racist” myself, but a lot of this really seems pretty stupid…like myth-making for identity politics.
i knew the pre-WN richard spencer (we lost touch after his ideological changes ~2010). he’s smart. i have a hard time believing he doesn’t know the latest research, which was evening starting to be evident back then. so i think it’s myth-making.
p.s. a friend of mine sent me a link to a richard spencer interview with kevin macdonald last year i think, pointing to a specific segment of the podcast talking about ancient genetics. kevin was telling richard how europeans 40,000 years ago were white, and those are the ancestors of europeans. that’s wrong.
Europeans 40kya were not white those in the area at that time are *not* the ancestors of today’s Europeans.
Both Afrocentrists and Nordicists need to keep up with the new information that’s constantly coming out. Because what they say in regards to genetics and/or anything else is mostly wrong.
Edit, 7/18/17: r/K selection theory has been rebutted.
r/K theory doesn’t apply to humans and if it did, Mongoloids would be r and Africans would be K. Cold with is an agent of r selection while endemic disease is an agent of K selection. Rushton used a debunked “continuum” for the basis for his theory and completely changed r and K. However it’s wrong. Rushton was wrong. Anonymous Conservative is wrong. Anyone who uses those two in reference to r/K is wrong by proxy since r/K is a debunked paradigm.
Japan has had a population crisis for a few years. Japan’s fertility rate was 1.4 in 2014. To have enough children to keep the population stable, the Total Fertility Rate (TFR) needs to be 2.1. As a country industrializes and becomes more prosperous, the TFR drops as higher IQ follows better nutrition. As a nation industrializes and becomes more complex, the attention of the populace shifts from one of having children and a family to one of success and intellectualism. As this occurs, the birth rate drops because the more intelligent a population is, the more likely it is for them to pursue higher education or monetary achievement. Clearly, the main reason Japan has concerns with their TFR is due to their high intelligence.
The Japan Times reported yesterday that almost half of single young men and women were virgins. A survey of Japanese men and women aged 18-34 found that 70 percent of unmarried men and 60 percent of unmarried women were not in a relationship. Also discovered, 42 percent of the men and 42.4 percent of the women admitted to being virgins. The survey was taken before in 2010, with 36.2 percent of men and 38.7 percent of women admitting to being virgins.
These surveys have been carried out every 5 years since 1987. Then, the rate of men who said they had no partner was 48.6 percent and for women it was 39.5 percent. The survey, which was conducted last June and accounted for 8,754 single people and 6,598 married couples across Japan, also found that 90 percent of the respondents wanted to get married “sometime in the future”, but for some people, this turns out to be a mistake. Moreover, 30 percent of the 2,760 men and 26 percent of the 2,570 women polled said they were not currently looking for a relationship. The increase in singles was most noted in the 20s, when women are the most fertile. The Prime Minister of Japan, Shinzo Abe also said he wants to increase the birthrate from 1.4 to 1.8 by 2025.
Lastly, the study found that the number of children for couples marries for 15 to 19 years was 1.94, a record low. This study did not ask questions about same-sex partners, but what we are concerned about is the TFR and how it’s driven by evolution, so this is a non-factor.
Japan’s population is dramatically shrinking. In 2010, they had a population of 128 million but by their 2015 census, they had a population of 127 million. This is due to the increase in virgins and an aging population. Why is this happening?
This is, of course, driven by r/K Selection Theory. Rushton thought of r/K Selection Theory, also known as Differential K theory, in 1985 with a paper titled Differential K Theory: The Sociobiology of Individual and Group Differences. Organisms can be r-selected, K-selected or somewhere in between. Humans as a species are K-selected, but some human races and ethnies are more K-selected than others.
Africans are r-selected, meaning that they have many children while not investing too much time in their offspring. They evolved to be r-selected to offset the high mortality rate due to the harshness of Sub-Saharan Africa. Due to this, black girls have an earlier menarche (period) so they can reproduce more to a) offset the high mortality rate and b) have a chance to reproduce more due to the high mortality rate. This is driven by disease, malnutrition, and parasitic load, which also drop IQ and contribute to the high birth rate since lower IQ populations have more children.
Caucasians are in the middle of r and K, and have fewer children and put more energy into caring for each one. This goes back to evolving in the Ice Age where cooperation and altruism were needed. More attention to children was needed for Eurasians evolving back then due to the harsh conditions of the Ice Age. So, a higher IQ evolved, and along with the higher IQ came a bigger brain. The bigger brains of Eurasians led to children being born earlier, and a bigger brain allowed for better care for the children along with numerous other positive variables to help survive in the harsh weather. Moreover, genes from Neanderthals are responsible for a 1 percent decrease in historic fitness (biological fitness) in Eurasian populations.
Orientals (Japanese, Chinese, Koreans) are further K than Caucasians are. This is reflected in brain size, where more K-selected populations have bigger brains, thus they can think further into the future and maximize care for their children. The opposite holds true for blacks. This is reflected in modern-day, first-world life where blacks have too many children to care for on their own accord and whites and Orientals have fewer children and put more investment into their children .
It’s not only Japan that’s having this problem with birthrates. It’s all of the West and East Asia. Higher IQ societies do have a longer life expectancy, while lower IQ societies have a lower one. Then, as described above, the lower IQ populations have more children to offset the mortality rate.
Japan’s birthrate concerns are due largely in part to genetic factors. This is currently occurring in all high IQ populations. Those populations have a large elderly population, with the young demographic quickly shrinking. Seeing this gradient throughout the world with IQ and fertility rates, we can make some general conclusions:
- Low IQ populations have more children while high IQ populations have less children.
- High IQ populations are more likely to have a large subset of virgins, as seen with this article. Lower IQ populations lose their virginity earlier.
This can be seen with the CLASH (CLimate, Aggression and Self-control in Humans) model (Van Lange, Rinderu, and Bushmen 2016). According the the CIA World Fact book 2014, in countries closer to the equator, the average age of first birth for a female was 20 years of age (the countries were the Gaza strip, Liberia, Bangladesh, Kenya, Mali, Tanzania, Uganda and various other middle African countries). Conversely, for countries further away from the equator, the average age of first birth was 28 years of age (Japan, Canada, and most European countries). Those populations that evolved in warmer climates where the changes in season are minimal with unpredictable harshness tend to enact faster life history strategies than those in colder climates.
Moreover, a slower life history strategy (K-selection), under a predictable environment would be better to enhance inclusive fitness. There is a growing body of evidence that predictable environments promote K-selection “in terms of lower mortality, morbidity, delayed reproduction, and a higher contribution towards one’s social capital.” This can be seen with the trends in Western and East Asian countries.
The trend that Japan is facing can be reversed with incentives for reproduction. However, the more intelligent a society is, the fewer children it will have due to evolutionary pressures. Is there a happy medium between IQ and fertility rates, where the population isn’t too dumb and the fertility rates aren’t too low? I’ll explore that in the future.