The primary focus of research in my lab has been understanding the mechanistic basis for variation in individual performance and life history. To this end, we can categorize our work as followings:


Understanding of the role of mitochondrial function and reactive oxygen species exposure in reproduction and longevity.

In the last few years, the lions-share of our work has focused on understanding the mechanisms that underlie the tradeoff between reproduction and longevity. In other words, we want to know why is it that species and individuals with higher reproductive output tend to have a shorter lifespan than those with lower reproductive output. We have taken several approaches to addressing this question: 


  • The relationship between reproduction, oxidative stress, mitochondrial function, and subsequent survival 

    • We have evaluated the impact of litter size on overwinter survival in Columbian ground squirrel. (Amy L. Skibiel et al., 2013)

    • We evaluated how reproduction changes oxidative stress and mitochondrial performance during and after reproduction in wild-derived house mice, lab mice, and lab rats. (Hyatt et al., 2018a; Hyatt et al., 2018b; Mowry et al., 2017, 2016; Park et al., 2020) 

    • We evaluate the relationship between the expression of a sexually selected trait and oxidative stress and mitochondrial performance in the house finch. (Hill et al., 2019)


Current summary: Our results currently provide no evidence that reproduction has immediate impacts on survival or that reproduction hinders the immediate performance of mitochondria, even under enhanced oxidative damage.  


  • The interaction between oxidative events and life history


Animals experience many events that can alter their oxidative balance – including but not limited to heat stress, pathogens, toxins, relative activity, and reproduction. We ask these events interact to alter individual performance. We suspect that these interactions contribute to variation in performance among individuals. 


  • We have quantified the impact of relative ROS exposure on reproductive performance and longevity and on mitochondrial physiology. (Heine et al., 2019; Zhang et al., 2018a)

  • We have asked how reproduction impacts a females ability to respond to a subsequent oxidative event. (Wendy R. Hood et al., 2019)


Current summary: Our findings highlight the relative ROS exposure does interact with the life history patterns of animals, and this response appears to be linked to changes in the mitochondria.


  • The response of mitochondria to ROS exposure

  • We have directly altered ROS production in animals to evaluate how the mitochondria respond to an oxidative event. (Zhang et al., 2018b)

Current summary: We have found that both mitochondrial physiology and mitochondrial morphology response to increased ROS. While the initial insult increases oxidative damage and hinders mitochondrial respiration but both recover. Both ROS levels drop, and the enzymatic activity of the mitochondrial complexes improves. Our results highlight that it is important to consider the timing and dosage of ROS in any study. 


  • Theory on the mechanistic basis for life-history tradeoffs


  • We have written theoretical papers proposing a role for mitochondrial hormesis in life-history tradeoff and a possible role of mitochondrial replication error in the life history patterns of animals in the wild. (Hood et al., 2018; Wendy R Hood et al., 2019; Zhang and Hood, 2016)


Does endoplasmic reticulum stress influence performance in natural contexts?


  • Endoplasmic reticulum stress occurs when unfolded proteins accumulate within the ER. Cells respond by upregulating the unfolded protein response (UPR). Variation in the performance of the UPR had been correlated to variation in the condition of laboratory animals, and a poor functioning UPR has been linked to several diseases such as Alzheimer's and Parkinson's disease. We currently have no understanding of how variation in the UPR impacts animals' performance in the wild.


Milk composition and the impact of lactation on human health


  • We have described milk composition for several species, including naked-mole rats, Columbian ground squirrels, and several species of bats. (Hood, 2001; Hood et al., 2001, 2014; Kunz and Hood, 2000; Skibiel and Hood, 2012)

  • We have shown that the composition of a mother's milk composition impacts offspring survival in Columbian ground squirrels. (Skibiel and Hood, 2015)

  • We completed the first phylogenetically corrected statistical analysis of milk composition across vertebrates, allowing us to describe factors that contribute to the evolution of milk composition. (A L Skibiel et al., 2013)

  • We have described how maternal diet impacts milk microbiota. (Warren et al., 2019)

  • In humans, women who do not nurse their babies have a higher statistical probability of obesity, diabetes, and cancer than women who forgo nursing. We have quantified the impact of lactation on cellular metabolism and mitochondrial function. (H. W. Hyatt et al., 2018; Hyatt et al., 2017) 



Do animals maintained in seminatural enclosures display phenotypes that are more closely related to animals living in the wild than animals living under standard laboratory conditions?


The phenotypes that animals display are a product of gene by environmental interactions. Thus, to get accurate phenotype measures, we think it's important to evaluate phenotype under natural context. When we can't study animals in the wild, we often kept them in enclosures designed to mimic the animal's natural environment. 

We are currently evaluating if the white-footed phenotypes in our seminatural enclosure are more similar to wild mice than mice living in laboratory conditions.





Heine, K.B., Powers, M.J., Kallenberg, C., Tucker, V.L., Hood, W.R., 2019. Ultraviolet irradiation increases size of the first clutch but decreases longevity in a marine copepod. Ecol. Evol. 9, 9759–9767.

Hill, G.E., Hood, W.R., Ge, Z., Grinter, R., Greening, C., Johnson, J.D., Park, N.R., Taylor, H.A., Andreasen, V.A., Powers, M.J., Justyn, N.M., Parry, H.A., Kavazis, A.N., Zhang, Y., 2019. Plumage redness signals mitochondrial function in the house finch. Proc. R. Soc. B Biol. Sci. 286.

Hood, W.R., 2001. Nutritional Limitations on Lactation and Postnatal Growth in the Big Brown Bat, Eptesicus fuscus. Boston University, Boston, MA.

Hood, W.R., Kunz, T.H., Oftedal, O.T., Iverson, S.J., LeBlanc, D., Seyjagat, J., 2001. Interspecific and intraspecific variation in proximate, mineral, and fatty acid composition of milk in old world fruit bats (Chiroptera : Pteropodidae). Physiol. Biochem. Zool. 74, 134–146.

Hood, Wendy R, Williams, A.S., Hill, G.E., 2019. An ecologists’ guide to mitochondrial DNA mutations and senescence. Integr. Comp. Biol.

Hood, W.R., Zhang, Y., Mowry, A. V, Hyatt, H.W., Kavazis, A.N., 2018. Life History Trade-offs within the Context of Mitochondrial Hormesis. Integr. Comp. Biol.

Hood, Wendy R., Zhang, Y., Taylor, H.A., Park, N.R., Beatty, A.E., Weaver, R.J., Yap, K.N., Kavazis, A.N., 2019. Prior reproduction alters how mitochondria respond to an oxidative event. J. Exp. Biol. 222, jeb.195545.

Hood, W.R., Kessler, D.S., Oftedal, O.T., 2014. Milk composition and lactation strategy of a eusocial mammal, the naked mole-rat. J. Zool. 293, 108–118.

Hyatt, H.W., Zhang, Y., Hood, W.R., Kavazis, A.N., 2018. Changes in metabolism, mitochondrial function, and oxidative stress between female rats under nonreproductive and 3 reproductive conditions. Reprod. Sci. 

Hyatt, H.W., Zhang, Y., Hood, W.R., Kavazis, A.N., 2017. Lactation has persistent effects on a mother’s metabolism and mitochondrial function. Sci. Rep. 7, 17118.

Hyatt, H.W., Zhang, Y., Hood, W.R., Kavazis, A.N., 2018. Physiological, mitochondrial, and oxidative stress differences in the presence or absence of lactation in rats. Reprod. Biol. Endocrinol. 16, 2–14.

Kunz, T.H., Hood, W.R., 2000. Parental care and postnatal growth in the Chiroptera, in: Krutzsch, P.H., Creichton, E.G. (Eds.), Reproductive Biology of Bats. Academic Press, New York, pp. 415–468.

Mowry, A. V., Donoviel, Z.S., Kavazis, A.N., Hood, W.R., 2017. Mitochondrial function and bioenergetic trade-offs during lactation in the house mouse (Mus musculus). Ecol. Evol. 7, 2994–3005.

Mowry, A. V., Kavazis, A.N., Sirman, A.E., Potts, W.K., Hood, W.R., 2016. Reproduction Does Not Adversely Affect Liver Mitochondrial Respiratory Function but Results in Lipid Peroxidation and Increased Antioxidants in House Mice. PLoS One 11, e0160883.

Park, N.R., Taylor, H.A., Andreasen, A., Williams, A.S., Niitepõld, K., Yap, K.N., Kavazis, A.N., Hood, W.R., 2020. Mitochondrial physiology varies with parity and body mass in the laboratory mouse. J. Comp. Physiol. - B Biochem. Syst. Environ. Physiol.

Skibiel, A L, Downing, L.M., Orr, T.J., Hood, W.R., 2013. The evolution of the nutrient composition of mammalian milks. J Anim Ecol 82, 1254–1264.

Skibiel, A.L., Hood, W.R., 2015. Milk matters: offspring survival in Columbian ground squirrels is affected by nutrient composition of mother’s milk. Front. Ecol. Evol. 3.

Skibiel, Amy L., Speakman, J.R.., Hood, W.R., 2013. Testing the predictions of energy allocation decisions in the evolution of life-history trade-offs. Funct. Ecol. 27, 1382–1391.

Skibiel, A.L.A.L., Hood, W.R.W.R., 2012. Milk composition in a hibernating rodent, the Columbian ground squirrel (Urocitellus columbianus). J. Mammal. 94, 146–154.

Warren, M.F., Hallowell, H.A., Higgins, K. V., Liles, M.R., Hood, W.R., 2019. Maternal dietary protein intake influences milk and offspring gut microbial diversity in a rat (Rattus norvegicus) model. Nutrients 11.

Zhang, Y., Brasher, A.L., Park, N.R., Taylor, H.A., Kavazis, A.N., Hood, W.R., 2018a. High activity before breeding improves reproductive performance by enhancing mitochondrial function and biogenesis. J. Exp. Biol. 221, jeb.177469.

Zhang, Y., Hood, W.R., 2016. Current versus future reproduction and longevity: a re-evaluation of predictions and mechanisms. J. Exp. Biol. 219, 3177–3189.

Zhang, Y., Humes, F., Almond, G., Kavazis, A.N., Hood, W.R., 2018b. A mitohormetic response to pro-oxidant exposure in the house mouse. Am. J. Physiol. - Regul. Integr. Comp. Physiol. 314, R122–R134.



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